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Objective To investigate changes and clinical significance of serum microRNA-155 (miR-155) and microRNA-205-5p (miR-205-5p) levels in patients with hepatitis C virus (HCV) infection. Methods A total of 141 patients with HCV infection were collected and divided into the HCV-1b group (92 cases) and the non HCV-1b group (49 cases) according to their genotype, and another 141 healthy volunteers who underwent physical examinations in our hospital during the same period were collected as the control group. The general information, biochemical indicators and serum levels of miR-155 and miR-205-5p were compared between the three groups. According to the grading of hepatitis activity, HCV infected patients were classified into the G0, G1, G2, G3 and G4 groups, and serum levels of miR-155 and miR-205-5p were compared between the five groups. Receiver operating characteristics (ROC) curve was used to analyze clinical values of serum miR-155 and miR-205-5p in diagnosing hepatitis activity of G1-G4 in patients with HCV infection. Results The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin (TBIL) were obviously higher in the HCV-1b group and the non HCV-1b group than those in the control group, while the level of ALB was obviously lower than that in the control group (P＜0.05). The serum level of miR-155 was increased in turn in the control group, the nonHCV-1b group and the HCV-1b group, and the serum level of miR-205-5p was decreased in turn (P＜0.05). The serum level of miR-155 increased in turn with the increased grading of hepatitis activity, while the serum miR-205-5p level decreased in turn (P＜0.05). The area under curve (AUC) values of serum miR-155, miR-205-5p and their combination in diagnosing hepatitis activity of G1-G4 in HCV infected patients were 0.855, 0.793 and 0.913, respectively, and the combination of the two is superior to each individual diagnosis (P＜0.05). Conclusion The serum miR-155 level increases and miR-205-5p level decreases in HCV infected patients. The combination of the two has high efficacy in diagnosing hepatitis activity of G1-G4 in HCV infected patients. [ABSTRACT FROM AUTHOR]

Glioma is the most malignant brain tumor with high mortality. Due to its complex biological characteristics such as malignant proliferation, invasion, drug resistance, and immunosuppression, the clinical treatment faces great difficulties. Although the survival rate has improved under surgery combined with radiotherapy and chemotherapy, the overall curative effect is still not obvious. As a kind of non coding RNA (ncRNA), microRNA (miRNA) which has been extensively studied in recent years is involved in the regulation of biological processes of normal tissues and various tumors (including glioma) in human. As a cancer suppressor gene, miRNA - 145 plays a regulatory role in the progression of glioma through a variety of pathways, especially as a targeted drug transported to the tumor area through nanocarriers to treat tumors, becoming a current research hotspot. This article summarizes the role of miRNA - 145 in pathological grading, tumor microenvironment, the regulation of glioma stem cells, drug resistance, and the prognosis of glioma, aiming to provide the reference for the diagnosis and treatment of glioma. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of miR-181c-5p on vasculogenic mimicry (VM) in ovarian cancer stem-like cells (OCS-LCs) and its mechanism. Methods OVCAR3 cells were induced into OCS-LCs by serum-free suspension culture. OVCAR3 cells were divided into groups A, B, and C and were transfected with NC-miR-181c-5p, siRNA-miR-181c-5p, and pRNA-miR-181c-5p, respectively. The sphere-forming experiment was used to assess the sphere formation ability of groups A, B, and C. RT-qPCR was used to measure the relative expression level of miR-181c-5p in cells of groups A, B, and C, and Western blot was used to measure the relative protein expression levels of Oct-4, Nanog, HIF-1α, and VEGF in cells of groups A, B, and C. CCK-8 assay was used to measure the viability of cells in groups A, B, and C, and the three-dimensional culture experiment was used to measure the angiogenesis rate of groups A, B, and C. Results OVCAR3 cells were successfully induced into OCS-LCs. RT-qPCR showed that group B had a significantly lower relative expression level of miR-181c-5p than group A, and group C had a significantly higher relative expression level than group A (t=2.25,8.68,P

Objective To investigate the regulatory effect of miRNA-933 on the apoptosis and proliferation of human hepatic stellate cell line LX-2 and its mechanism. Methods Firstly, with human liver tissue for research, gene micmarray technology was used to detect the differentially espressed genes in liver tissue between liver cirrhosis/chronic hepatitis B tissue and normal liver tissue, among which the significantly differentially expressed miRNAs were identified, and thus miltNA-933 was determined as the research object. Then, with the human hepatic stellate cell line LX-2 for research, miRNA-933 mimic and inhibitor (miRNA-933 siRNA) were used to construct the LX-2 models of overexpression and knockdown, and the cells transfected with mimic-NC (overexpression) or siRNA-NC (knockdown) were established as the negative control group. Quantitative real-time PCR and Western blot were used to measure the expression levels of miRNA-933 and activation biomarkers; techniques such as cell proliferation assay and flow cytometry were used to investigate the effect and mechanism of miRNA-933 on cell apoptosis. proliferation, and activation. The independent-samples i test was used for comparison of contimaous data between two groups; a une way analysis of variance was used for comparison between multiple groups, and Bonferroni correction was also performed. Results A total of 18 significantly differentially expressed miRNAs were obtained based on the results of gene microarray, among which miRNA-933 was significantly downregulated (P<0.05). After LX-2 cells were transfected with miRNA-933 mimiy or siRNA. compared with the negative conttul group, milINA-933 siRNA significantly downregulated the expression of miRNA-933 (P=0.0007), while miRNA-933 mimic significantly upergulated the expression of miRNA-933 (P=0.000 3). Western blot and quantitative real- time PCR showed that miRNA-933 siRNA significantly upregulated the expression of collagen 1 and a SMA (P<0.001), while miRNA-933 mimic significantly inhibited the expression of collagen 1 and -SMA (P<0.05). Flow cytometry showed that compared with the negative control group, miRNA-933 siRNA significantly downregulated the apoptosis rate of LX-2 cells (P=0.031 9), and miRNA-933 mimic significantly upregulated the apoptosis rate of LX-2 cells (P=0.005.5), Western blot showed that compared with the negative control group, miRNA-933 siRNA could inhibit the expression of Caspase-3 (-0.006 7) and poly (ADP-ribuse) polymerase-1 (PARP-1) (P=0.0030) and upregulate the expression of B-cell lymphoma-2 (Bel-2) in LX-2 cells (P=0.0020), while miRNA-933 mimie could significantly upregulate the expression of Caspase-3 (P=0.0118) and PARP-1 (P=0.049 5) and downregulated the expression of Bel-2 (P=0.002 1). Cell proliferation assay showed that compared with the negative control group. miRNA-933 siRNA could promote the proliferation of LX-2 cells (P=0.0115), while on the contrary, miRNA-933 minic could inhibit the proliferation of LX-2 cells (P=0.001 2). Western blot and quantitative real-time PCR showed that miRNA-933 IRNA significantly inhibited the expression of Kruppel-like factor 6 (KLF6) and downregulated the expression of activating transcription factor 4 (ATF4), activating transcription factor 3 (ATF3), and C/ERP homologous protein (CHOP), while miRNA-933 mimie promoted the experssion of the above proteins (all P<0.05). Conclusion This study shows that miRNA-933 may promote cell apoptosis and inhibit cell activation and proliferation by promoting the activation of the KLF6/ATF4/ATF3/CHOP/Bel-2 signal axis in LX-2 cella, [ABSTRACT FROM AUTHOR]

Copyright of Journal of Guangdong Pharmaceutical University is the property of Journal of Guangdong Pharmaceutical University and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the effect of oxaliplatin on the activation of hepatic stellate cells (HSCs), as well as the association of oxaliplatin with microRNA-30a-5p and autophagy. Methods HSC-LX2 cells were cultured and divided into groups according to the following three protocols： control group, PDGF treatment group, oxaliplatin treatment group, oxaliplatin+PDGF treatment group; control group, microRNA-30a-5p transfection group, PDGF treatment group, microRNA-30a-5p transfection+ PDGF treatment group; control group, 3-MA group, microRNA-30a-5p inhibitor group, microRNA-30a-5p inhibitor+3-MA group. Western Blot was used to measure the expression of HSC activation-related proteins (Collagen-I and alpha-smooth muscle actin [αSMA]) and HSC autophagy-related proteins (Beclin-1, P62, and LC3B); LysoTracker staining and immunofluorescence assay were used to measure the expression of LC3B autophagosomes; RT-PCR was used to measure the expression level of microRNA30a-5p; bioinformatics techniques were used to predict the potential targets of microRNA-30a-5p in HSCs. The independent samples t test was used for comparison of normally distributed continuous data between two groups; a one-way analysis of variance was used for comparison between multiple groups, and the least significant difference t-test was used for further comparison between two groups. Results After the cells were treated with oxaliplatin, RT-PCR results showed that the oxaliplatin treatment group had a significantly higher expression level of microRNA-30a-5p than the control group (P<0.01); Western Blot showed that the oxaliplatin treatment group had significant reductions in the expression levels of the HSC activation-related proteins α-SMA and Collagen-Ⅰ and the autophagy-related proteins Beclin 1 and LC3BⅡ/Ⅰ(all P<0.001); immunofluorescence assay showed that the oxaliplatin treatment group had a significantly lower number of autophagosomes than the control group (P<0.05). After HSCLX2 cells were transfected with microRNA-30a-5p mimic, compared with the control group, the microRNA-30a-5p mimic group had significant reductions in the expression levels of the autophagy-related proteins Beclin 1 and LC3BⅡ/Ⅰ(P<0.05) and the HSC activation-related protein Collagen-Ⅰ(P<0.001); after HSC-LX2 cells were transfected with microRNA-30a-5p inhibitor, Western Blot showed that compared with the control group, the microRNA-30a-5p inhibitor group had significant increases in the expression levels of the HSC activation-related proteins Collagen-Ⅰ and α-SMA and the autophagy-related protein Beclin 1(t= 2.41, 2.32, and 4.57, all P<0.05). Western Blot showed that compared with the control group, the microRNA-30a-5p inhibitor group had significant increases in the expression levels of the HSC autophagy-related protein Beclin 1 and the HSC activation-related protein α -SMA (both P<0.05), and after the treatment with the autophagy inhibitor 3-MA, there were no significant differences in the expression of these proteins between the two groups (P>0.05). The bioinformatics analysis using TargetScan, PicTar, and miRanda databases showed that the autophagy-related protein Beclin-1 might be a potential target of miRNA-30a-5p. Conclusion Oxaliplatin can inhibit the activation of HSCs by upregulating the expression of microRNA-30a-5p, which provides new ideas and a new target for the treatment of liver fibrosis. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) have emerged as key regulators of diverse biological processes, including cell proliferation, differentiation, apoptosis, and metabolism. They are also actively involved in the reproductive and developmental processes of organisms. Among the let-7 family, miR-202 stands out owing to its high conservation across different species, implying the potential shared functions and regulatory roles. Substantial evidence from numerous studies underscores the involvement of miR-202 in a wide range of pathophysiological processes. Notably, it exerts significant inhibitory effects on tumor cell proliferation, migration, and invasion. Moreover, miR-202 plays a critical role in modulating the differentiation of T cell and exhibits the implications in the regulation of neurodevelopment and neurodegenerative diseases. The increasing evidence have indicated that miR-202 plays a crucial role in gamete development and the regulation of reproductive physiology. In this article, we review the regulatory roles of miR-202 in key reproductive processes, namely spermatogenesis, follicle development, and reproductive endocrine regulation. [ABSTRACT FROM AUTHOR]

Oral submucous fibrosis (OSF) is one of the most common precancerous lesions of the oral mucosa, and its pathogenesis has not been fully elucidated. Small noncoding RNAs (SncRNAs), a class of RNA molecules that do not code for proteins, have been widely reported to be involved in the regulation of a variety of human diseases. An increasing number of studies have shown that a variety of SncRNAs play important roles in the pathogenesis of OSF. Current studies have shown that microRNAs (miRNAs) are involved in OSF disease progression by regulating the expression of related transcription factors and genes or epithelial mesenchymal transformation to regulate the activation of fibroblasts (FBs). Long noncoding RNAs (lncRNAs) that transform growth factor-β/suppressor of mothers against decapentaplegic (TGF-β/Smad) signaling pathways or interact with miRNAs are involved in the development of OSF. Circular RNAs (circRNAs) play a role in OSF by interacting with miRNAs. tRNA-derived small RNAs (tsRNAs) are involved in the progression of various fibrotic diseases, but their specific mechanism of action in OSF still needs to be further explored. In the future, it is still necessary to focus on the targets of SncRNAs mediating OSF progression and explore their function and molecular mechanism in OSF to provide new ideas for the diagnosis and treatment of OSF.

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Pancreatic cancer is a relatively common tumor of the digestive system， with difficulties in early-stage diagnosis and an extremely high degree of malignancy. Molecular diagnostic technology based on tumor biomarkers， combined with the existing gold standard in clinical practice， is of great clinical significance to achieve early accurate identification， timely treatment and intervention， and reduction in mortality. Previous studies have shown that miRNAs show high specificity in terms of types and expression levels in different pathological stages of pancreatic cancer and can thus be used in monitoring the development and progression of pancreatic cancer. Since a single miRNA has a limited diagnostic potential， the combination of different miRNAs may effectively improve the diagnostic efficiency of early-stage pancreas carcinogenesis. Based on related research advances in recent years， this consensus document aims to fill the gap in molecular diagnostic technology in the guidelines for the clinical diagnosis and treatment of pancreatic cancer and provide expert guidance and recommendations. [ABSTRACT FROM AUTHOR]

Cervical cancer, endometrial cancer and ovarian cancer are the three most common malignant tumors in gynecology, and the incidences are on the rise in all ages in recent years. The gynecological malignant tumors have become a serious threat to women's health in China. Although the application of a variety of targeted drugs has significantly prolonged the survival of patients, cervical cancer, endometrial cancer and ovarian cancer are still a group of diseases that cannot be accurately diagnosed and treated. MiR-17-92 gene cluster, as the earliest identified miRNA family of oncogene, has been widely concerned about its mechanism. As a member of the miR-17-92 gene cluster, miR-20a can play a post-transcriptional regulatory role by reducing or increasing the expression, thus affecting the downstream gene pathway, regulating the proliferation, invasion, and metastasis of malignant tumor cells, and finally achieving the occurrence and progress of malignant tumors. According to the current research progress, the specific increase of miR-20a expression in cervical cancer, endometrial cancer and ovarian cancer is usually related to the malignant progress of the disease. This article reviews the research progress of miR-20a in the pathogenesis of three common gynecological malignant tumors. [ABSTRACT FROM AUTHOR]

Objective To explore the relationship between serum miRNA-21 and miR-27b levels and prognosis of patients with renal clear cell carcinoma. Methods A total of 118 patients with renal clear cell carcinoma admitted to the Qinghai University Hospital from February 2019 to April 2021 were selected as the study subjects, and another 118 healthy patients in the same period as the control group. Real time fluorescence quantitative polymerase chain reaction ( PCR) was used to detect the expression of miR-21 and miR-27b in the serum of all subjects. The relative expression levels of serum miR-21 and miR-27b between the patients with renal clear cell carcinoma and healthy control patients were compared. The expression and correlation of serum miR-21 and miR-27b in the patients with renal clear cell carcinoma of different pathological stages and Fuhrman grading were analyzed. The relationship between the expression of serum miR-21 and miR-27b and the survival and prognosis of the patients was explored as well. Results The expression levels of serum miR-21 and miR-27b in the patients with renal clear cell carcinoma were higher than those in the healthy control group (P < 0.05). The serum miR-21 expression level in stage IE patients was higher than in stage I (P < 0.05), while the serum miR-21 expression level in the stage IV patients was higher than that in stages I, II, and IE (P < 0.05). The expression level of miR-27b in the serum of patients gradually increased across the four stages, with a significant difference (P < 0.05). The pathological staging was positively correlated with the expression of miR-21 and miR-27b (P < 0.001). The expression levels of miR-21 and miR-27b in serum of patients gradually increased across grades I, E and IE by Fuhrman grading, with significant difference (P < 0.05). Fuhrman grading was positively correlated with the serum miR-21 and miR-27b expression (P < 0.001). There was a statistically significant difference in the survival curve between the miR-21 high expression group and the low expression group ( P < 0.05 ) . There was a statistically significant difference in the survival curve between the high expression group and the low expression group of miR-27b (P < 0.05). Conclusion The expression levels of serum miR-21 and miR-27b in patients with renal clear cell carcinoma is indicative of the progression and prognosis of the patient's condition. [ABSTRACT FROM AUTHOR]

The aberrant activation of yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), downstream effectors of the Hippo signaling pathway, has been implicated in hepatocellular carcinoma(HCC). The microRNAs (miRNAs) works as a tumor suppressors that influence the proliferation, migration and apoptosis of tumor cells by modulating Hippo-YAP/TAZ signaling during hepatic tumorigenesis. Exploring the role of miRNAs in regulating Hippo YAP/TAZ pathway in HCC can provide new ideas for the diagnosis and treatment of HCC.

MicroRNAs(miRNAs) are involved in the pathophysiological processes of many diseases. Stably present in cells, tissues and blood, they can be used as potential markers of many diseases. They play an important role in the pathogenesis of liver fibrosis caused by various chronic liver diseases. It has been shown that miRNAs can participate in the process of liver fibrosis by targeting the down-regulation of liver fibrosis-related gene expression. In this review, we discuss the research progress on the role of miRNAs in liver fibrosis, with the hope of providing reference for diagnosis and molecularly targeted treatment.

Objective To investigate the feasibility of constructing a preeclampsia (PE) risk model based on multiple exosomal micrornas (miRNA) expression levels and to verify its efficacy in predicting PE. Methods A total of 1 037 pregnant women who were archived in our hospital from June 2019 to December 2021 and whose gestational weeks were less than or equal to 20 weeks were selected as the research subjects. The expression of exosomal miRNA (including miR-155- 5p, miR-215-5p, miR-203a-3p, miR-199a-5p and miR-125a-3p) in all samples was detected by qRT-PCR. Then, all patients were followed up to the end of pregnancy. The occurrence of PE during the follow-up period was counted, and all samples were divided into the PE group and the control group according to results. Cox regression was used to analyze the influencing factors of PE. The multi-miRNA risk model was constructed with ggrisk package, and the predictive effect of the model on PE was evaluated by receiver operating characteristic (ROC) curve. Results By the end of follow-up on October 31, 2022, 974 cases were finally followed up, and the follow-up completion rate was 93.92%. Among all the 974 patients who completed the follow-up, 65 patients developed PE, so they were finally divided into the PE group, and 909 cases were used as the control group. The age, pre-pregnancy BMI and waist circumference at 12 weeks of gestation were higher in the PE group than those in the control group (P＜0.05). The proportions of smoking history and drinking history were higher in the PE group than those of the control group (P＜0.05). The contents of triglyceride (TG), low density lipoprotein cholesterol (LDL-C), total cholesterol (TC), alanyl aminotransferase (ALT), aspartate aminotransferase (AST), platelet distribution width (PDW), mean platelet volume (MPV), miR-155-5p, miR-199a-5p and miR-215-5p were higher in the PE group than those in the control group，while contents of thyroid stimulating hormone (TSH), miR-125a-3p and miR-203a-3p were lower in the PE group than those in the control group (P＜0.05). The expression levels of miR-125a-3p, miR-155-5p, miR-199a-5p and miR-215-5p were independent predictors of PE (P＜0.05). The predictive risk model constructed from the above miRNAs had good predictive value in the occurrence of PE (AUC=0.998), with a sensitivity of 98.46% (63/65) and a specificity of 93.94% (854/909). Conclusion miR-125a-3p, miR-155-5p, miR-199a-5p, miR-203a-3p and miR-215- 5p are significantly related to the occurrence of PE, and the PE prediction model constructed with the above five miRNAs has better effect. [ABSTRACT FROM AUTHOR]

The aberrant activation of yes-associated protein（YAP） and transcriptional coactivator with PDZ-binding motif（TAZ）, downstream effectors of the Hippo signaling pathway, has been implicated in hepatocellular carcinoma（HCC）. The microRNAs（miRNAs） works as a tumor suppressors that influence the proliferation, migration and apoptosis of tumor cells by modulating Hippo-YAP/TAZ signaling during hepatic tumorigenesis. Exploring the role of miRNAs in regulating Hippo YAP/TAZ pathway in HCC can provide new ideas for the diagnosis and treatment of HCC. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of microRNA-223-3p （miR-223-3p） on hepatic stellate cell （HSC） activation and its mechanism. Methods Human HSC LX2 cells were selected for the study, and LX2 cells were stimulated by TGF- β to establish a model of HSC activation； quantitative real-time PCR was used to measure the change in the expression level of miR-223-3p during HSC activation. After LX2 cells were transfected with miR-223-3p mimic, quantitative real-time PCR, Western blot， and immunofluorescence assay were used to clarify the regulatory effect of miR-223-3p on HSC activation, and dual-luciferase reporter assay was used to verify the association between miR-223-3p and the target geneMAP1B. After LX2 cells were transfected with MAP1B siRNA, Western blot was used to clarify the influence of inhibiting MAP1B expression on HSC activation； after LX2 cells were transfected with miR-223-3p, quantitative real-time PCR and Western blot were used to verify the regulatory effect of miR-223-3p on MAP1B. The independent-samples t test was used for comparison of continuous data between two groups. Results HSC in the activated state had a significant reduction in the expression level of miR-223-3p compared with those in the resting state （t=9.12，P<0.001）. Overexpression of miR-223-3p inhibited the mRNA and protein expression levels of the markers for HSC activation alpha-smooth muscle actin and collagen type Ⅰ（mRNA expression：t=8.35 and 12.23, both P<0.01； protein expression：t=16.24 and 20.90， both P<0.001）. The dual-luciferase reporter assay confirmed that MAP1B was a potential target gene of miR-223-3p. Compared with the control group， LX2 cells with miR-223-3p overexpression had significant reductions in the mRNA and protein expression levels of MAP1B （mRNA expression：t=5.95，P<0.01； protein expression：t=11.12，P<0.001）. Conclusion This study shows that miR-223-3p can inhibit HSC activation by targeting MAP1B. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of miR-429 on the proliferation and migration of breast cancer cells and its mechanism. Methods RT-qPCR and Western blotting were used to measure the relative mRNA and protein expression levels of eIF4E in breast cancer MCF-7, MDA-MB-231, MDA-MB-468, and BT-549 cells and normal breast epithelial MCF-10A cells. MCF-7 cells were transfected with miR-429 mimics (group A), mimics NC (group B), miR-429 inhibitors (group C), and inhibitors NC (group D), and RT-qPCR, CCK-8 assay, wound healing assay, and Western blotting were used to measure the expression of miR-429, cell proliferation and migration, and the relative mRNA and protein expression levels of eIF4E in groups A-D. The 293T cells were transfected with eIF4E-3'UTR-Wt+miR-429 mimics (group E), eIF4E-3'UTR-Wt+mimics NC (group F), eIF4E-3'UTR-Mut+miR-429 mimics (group G), and eIF4E-3'UTR-Mut+mimics NC (group H), and relative luciferase activity was measured for groups E-H. The targeted regulatory effect of miR-429 on eIF4E was analyzed. Results RT-qPCR and Western blotting showed that the relative mRNA and protein expression levels of eIF4E in MCF-7, MDA-MB-231, MDA-MB-468, and BT-549 cells were significantly higher than those in normal breast epithelial MCF-10A cells (F=74.414,1 981.243,P

Objective To investigate the expression levels of serum exosomal miR-223 and nucleotide-binding oligome-rization domain-like receptor protein 3 (NLRP3) in patients with Alzheimer’s disease (AD) and their association with the development and progression of AD. Methods A total of 65 elderly patients with AD who attended Department of Geriatrics in our hospital from March 2018 to December 2019 were enrolled as study group and were divided into mild cognitive impairment (MCI) subgroup with 41 patients and dementia of Alzheimer type (DAT) subgroup with 24 patients, and 60 elderly individuals with normal neurological function were enrolled as control group. Quantitative real-time PCR and ELISA were used to measure the expression levels of serum exosomal miR-223 and NLRP3. The Pearson and Spearman tests were used to analyze the correlation of serum exosomal miR-223 and NLRP3 with Mini-Mental State Examination (MMSE) score. The receiver operating characteristic (ROC) curve was plotted to calculate the area under the ROC curve (AUC) of serum exosomal miR-223 and NLRP3 in the diagnosis of MCI in AD patients or the differential diagnosis of DAT. Results Compared with the control group, the study group had a significantly lower expression level of serum exosomal miR-223 and a significantly higher expression level of NLRP3 (t=6.623,Z=-9.451,P

Objective To investigate the effect of miR-663b on the inflammatory response and apoptosis of nucleus pulposus cells (NPCs) induced by interleukin-1β (IL-1β) and its mechanism. Methods According to the different treatment me-thods, NPCs were divided into group A (no treatment), group B (induced by IL-1β), group C (IL-1β induction+miR-663b mimic transfection), and group D (IL-1β induction+miR-633b NC transfection). RT-qPCR was used to measure the expression levels of miR-663b, inflammatory factors [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-1β], type Ⅱ collagen, and po-lysaccharide in NPCs; CCK-8 assay and TUNEL staining were used to observe the proliferation and apoptosis of NPCs; Western blotting was used to measure the protein expression level of interleukin-1 receptor 1 (IL1R1) in NPCs. TargetScan database was used to predict the potential binding sites between miR-663b and IL1R1. The 293T cells were divided into group E (transfected with IL1R1-wt plasmid+miR-663b mimic), group F (transfected with IL1R1-wt plasmid+miR-663b mimic), group G (transfected with IL1R1-mut plasmid+miR-663b mimic), and group H (transfected with IL1R1-mut plasmid+mimic NC), and the luciferase activity of NPCs was measured for each group. Results RT-qPCR results showed that compared with groups A, B, and D, group C had a significant increase in the relative expression level of miR-663b (t=9.41-22.93,P

Background There are numerous patients with diabetes complicated with heart failure. Dapagliflozin is a new hypoglycemic drug that has been used for heart failure according to guideline recommendation, however, its mechanism of improving heart function has not been fully defined. Objective To study the effects of dapagliflozin on the expression of plasma miRNA-423-5p and cardiac function in patients with type 2 diabetes mellitus (T2DM) and chronic heart failure (CHF) . Methods Fifty patients with T2DM complicated with CHF admitted to the 960th Hospital of PLA from April 1 to November 30, 2021 were enrolled and randomly divided into dapagliflozin group (n=25) and control group (n=25) . Both groups received the same treatment for six months except that dapagliflozin group received dapagliflozin 10 mg/d per day, and the control group received other hypoglycemic drugs. They were compared to healthy physical examinees with normal cardiac function (healthy group, n=25) . Basic data of the patients were collected through the electronic medical record system, including age, sex, smoking history, hypertension, blood pressure level, body mass index (BMI) , blood lipid, blood glucose, creatinine (Cr) , amino-terminal pro-B-type natriuretic peptide precursor (NT-proBNP) , alanine aminotransferase (ALT) , aspartate aminotransferase (AST) , NYHA class, results of cardiac color ultrasound and drug combination. Blood samples were collected for the detection of miRNA-423-5p. A six-month follow-up was given to the patients with the time of first administration of dapagliflozin after inclusion as the starting point, during which patients' cardiac function indices and miRNA-423-5p were measured and collected at the end of four weeks of treatment, and their cardiac function indices, blood pressure level, ALT, AST, and Cr were measured at six months of treatment. Pearson correlation analysis or Spearman rank correlation analysis was used to analyze the correlation between miRNA-423-5p expression level and cardiac function indices of the patients. Results After 6 months of intervention, left ventricular ejection fraction (LVEF) , stroke output (SV) and left ventricular short-axis shortening rate (LVFS) in daglizin group were higher than those in control group, while left ventricular end-diastolic diameter (LVEDD) was lower than those in control group (P

Objective To explore effects of Casticin (Cas) on the proliferation, invasion, migration and microRNA-378 (miR-378) /paired related homeobox 1 (PRRX1) axis of gastric cancer (GC) SGC-7901 cells. Methods SGC-7901 cells were treated with Cas at different concentrations (0, 5, 10, 20, 40 and 80 μmol/L) for 48 h, and the cell viability of SGC- 7901 was detected by tetrazole salt (MTT) method. SGC-7901 cells at logarithmic growth stage were divided into 7 groups: the control group, the Cas low concentration group (10 μmol/L), the Cas medium concentration group (20 μmol/L), the Cas high concentration group (40 μmol/L), the Cas high concentration+miR-378 small interfering RNA (siRNA) group (40 μmol/L Cas+miR-378 siRNA), the Cas high concentration+PRRX1 group (40 μmol/L Cas+PRRX1 overexpressed plasmid) and the Cas high concentration+miR-378 siRNA+PRRX1 group (40 μmol/L Cas+miR-378 siRNA+PRRX1 overexpression plasmid). Cell activity, colony formation number, apoptosis rate, invasion and migration ability of SGC-7901 cells were determined by MTT assay, colony formation assay, flow cytometry, Transwell chamber assay and scratch assay, respectively. Expression levels of miR-378 and PRRX1 protein in SGC-7901 cells were detected by fluorescence quantitative PCR and Western blot assay. Double luciferase assay verified the targeting relationship between miR-378 and PRRX1. Xenografted SGC-7901 cells were xenografted into nude mice to verify the anticancer activity of Cas and its effect on the expression of miR-378. Results The cell viability of SGC-7901 cells in Cas 10, 20, 40 and 80 μmol/L groups decreased in a concentration-dependent manner (P＜0.05), and 10, 20 and 40 μmol/L Cas were selected as the follow-up study concentration. Compared with the control group, the cell viability, colony formation number, invasion cell number, scratch healing rate and PRRX1 protein expression level of SGC-7901 cells in the Cas low, medium and high concentration groups were decreased successively (P＜0.05), while the apoptosis rate and the expression level of miR-378 were increased successively (P＜0.05). Compared with Cas high concentration group, the cell viability, colony formation number, invasion cell number, scratch healing rate and PRRX1 protein expression levels were increased in the Cas high concentration+miR- 378 siRNA group and the Cas high concentration+PRRX1 group, and the apoptosis rate was decreased (P＜0.05). The expression level of miR-378 in SGC-7901 cells was decreased in the Cas high concentration+miR-378 siRNA group (P＜ 0.05). Compared with the Cas high concentration+miR-378 siRNA group, the expression level of miR-378 in SGC-7901 cells was increased in the Cas high concentration+PRRX1 group (P＜0.05). Compared with the Cas high concentration+miR- 378 siRNA group and the Cas high concentration+PRRX1 group, the cell viability, colony formation number, invasion cell number, scratch healing rate and PRRX1 protein expression levels were increased in the Cas high concentration+miR-378 siRNA+PRRX1 group (P＜0.05), and the apoptosis rate was decreased (P＜0.05). In SGC-7901 cells, miR-378 could target the expression of PRRX1. Cas inhibited the growth of transplanted tumor and promoted the expression of miR-378 in nude mice (P＜0.05). Conclusion Cas may inhibit the proliferation, invasion and migration of SGC-7901 cells by regulating the miR-378/PRRX1 axis. [ABSTRACT FROM AUTHOR]

Myocardial infarction is one of the most lethal diseases, and the progression of the disease often leads to the occurrence of chronic heart failure. Therefore, it is very important to explore new treatment methods for the prognosis of myocardial infarction. Exosomes are nanoscale vesicles with a diameter of 30-150 nm released from cells or tissue fluid. The vesicles carry specific DNA, RNA, proteins, lipids, metabolic waste and other substances secreted by parental cells. As a potential treatment for myocardial infarction, it has long been confirmed in basic experiments. This article reviews the latest research progress of exosomes from different cells and tissues, engineered exosomes and exosome cell membrane fusion strategies in the treatment of myocardial infarction, and provides scientific evidence for the clinical application of exosomes. [ABSTRACT FROM AUTHOR]

Objective To discover key miRNAs and their target genes affecting the progression of prostate cancer by bioinformatics analysis. Methods The prostate cancer miRNA dataset GSE36802 and prostate cancer mRNA datasets GSE46602 and GSE69223 were obtained from the GEO database, and the differentially expressed miRNAs were screened by GEO2R, and the target genes were predicted using miRWalk and miRPathDB and the intersection sets were taken. Subsequently, prostate cancer-related differentially expressed genes were analyzed and intersected with predicted target genes to finally obtain differentially expressed genes. The differentially expressed genes were analyzed by GO and KEGG enrichment using DAVID database, protein-protein interaction network was constructed using String database, and the pivotal genes were screened by Cytoscape software and CytoHubba plugin and validated by GEPIA2 database. Results A total of four miRNAs were obtained that were upregulated in prostate cancer tissues, namely miR-145-3p, miR-205-5p, miR-31-5p, and miR-455-5p. 153 differentially expressed genes were finally obtained, which were mainly enriched in biological processes such as regulation of RNA polymerase II promoter regulation, signal transduction, cell adhesion, and in signal transduction such as metabolic pathway, cancer pathway, calcium signaling pathway. Ten alternative pivotal genes were obtained by protein interaction network, and the differential expression of pivotal genes was verified by using GEPIA2, and finally four pivotal genes were obtained including: IGF1, PPARGC1A, FGFR2, and DPT. Conclusion Four differentially expressed miRNAs and four pivotal genes were discovered to provide the potential target for subsequent clinical treatment and basic research. [ABSTRACT FROM AUTHOR]

Objective To investigate the expression and significance of miR-409-3p in hepatoma carcinoma cell lines and possible molecular mechanism. Methods Quantitative real-time PCR was used to measure the expression of miR-409-3p in normal LO2 hepatocytes and four hepatoma cell line (HepG2, BEL-7402, SMMC-7721, and MHCC-97H). Hepatoma HepG2 cells were transiently transfected with miR-409-3p mimics and microRNA mimics control using the cationic liposome method, and then CCK8, plate colony formation assay, and flow cytometry were used to observe the effect of miR-409-3p on the proliferation, cell cycle, and apoptosis of hepatoma cells in vitro. Western blot was used to measure the change in the expression of c-Met protein in HepG2 cells with overexpression of miR-409-3p, and luciferase reporter gene assay was used to identify targeting relationship. The independent-samples t test was used for comparison between two groups, and a one-way analysis of variance was used for comparison between multiple groups, followed by the SNK test. Results Based on the TCGA microRNA expression profile data of liver cancer, the expression level of miR-409-3p in liver cancer tissue was significantly lower than that in adjacent tissue (t=7.752, P＜0.05). Compared with the LO2 cells, the HepG2, SMMC-7721, MHCC-97H, and BEL-7402 cells had a significant reduction in the expression level of miR-409-3p (F=31.043, P＜0.05). Compared with the miR-con group, the HepG2 cells transfected with miR-409-3p mimics had a significant increase in the expression level of miR-409-3p (t=-8.836, P＜0.05), suggesting that the interference was effective. CCK8 assay showed that compared with the miR-con group, the HepG2 cells transfected with miR-409-3p mimics had a significant reduction in proliferative capacity at 48, 72, and 96 hours (t=2.876, 3.359, and 3.707, all P＜0.05). Plate colony formation assay showed that the miR-409-3p mimics group had a significantly lower plating efficiency than the miR-con group (t=2.846, P=0.047). Flow cytometry showed that compared with the miR-con group, overexpression of miR-409-3p resulted in the increased number of HepG2 cells in G2 phase (t=-3.763, P＜0.05), while there was no significant difference in apoptosis rate (t=0.714, P=0.515). Luciferase reporter gene assay showed that c-Met was a target gene of miR-409-3p (t=4.970, P=0.007). Compared with the miR-con group, the HepG2 cells transfected with miR-409-3p mimics had a significant reduction in the expression of c-Met protein (t=-8.509, P=0.001). Conclusion By inhibiting the protein expression of c-Met, miR-409-3p regulates downstream signaling pathways to induce cell cycle arrest in G2 phase and thus inhibits the proliferation of hepatoma HepG2 cells. [ABSTRACT FROM AUTHOR]

Objective To investigate the differences in plasma exosomal microRNA (miRNA) expression profile between patients with chronic hepatitis B (CHB) and those with hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF), as well as their functions and biological processes, and to provide a reference for the clinical diagnosis of HBV-ACLF. Methods Six patients with CHB who were hospitalized in Department of Infectious Diseases, Qingdao Municipal Hospital, and six patients with HBV-ACLF who were treated in Blood Purification Center of Qingdao Sixth People’s Hospital from October 2021 to June 2022 were enrolled. Illumina high-throughput sequencing was used to analyze the plasma exosomal miRNAs of these patients to obtain the differentially expressed miRNAs between the two groups. The differentially expressed miRNAs were screened, and a functional enrichment analysis was performed to identify the biological processes involving such miRNAs. The Mann-Whitney U rank sum test was used for comparison of continuous data between two groups, and the chi-square test was used for comparison of categorical data between groups. Results A total of 249 differentially expressed exosomal miRNAs were obtained according to the criteria of upregulation ＞2-fold or downregulation ＞2-fold, with P＜0.05, and compared with the CHB group, there were 126 upregulated miRNAs and 123 downregulated miRNAs. The bioinformatics analysis showed that these differentially expressed miRNAs were mainly involved in the biological processes such as gonadal development, regulation of protein stability, and cellular response to external stimuli, and they were closely associated with the signaling pathways such as hepatitis B, the role of proteoglycans in cancer, regulation of stem cell pluripotency, MAPK, Hippo, TNF, and lipid metabolism. Conclusion The differentially expressed miRNAs identified by Illumina high-throughput sequencing may be used as biomarkers for the early diagnosis and prognostic evaluation of HBV-ACLF. [ABSTRACT FROM AUTHOR]

Objective To investigate the regulation and mechanism of circFAT1 on proliferation, invasion and epithelial-mesenchymal transition (EMT) of glioblastoma (GBM). Methods Fifty GBM samples and 5 non-tumor brain tissue (NBT) samples were collected, and 3 GBM and 3 NBT samples were randomly selected for tissue RNA sequencing. The expression levels of circFAT1 in U87, U251, T98G, LN229 GBM cell lines and NHA astrocyte lines were detected by qRT-PCR. The cyclic properties of circFAT1 were determined by selective degradation of linear transcripts by RNase R. GBM cells were divided into the sh-control group and the sh-circFAT1 group. Cell proliferation, invasion and EMT were detected by colony formation assay, transwell assay and Western blot assay after lentivirus transfection. Fluorescence in situ hybridization (FISH) was used to detect the localization of circFAT1 in GBM cells, and the interaction between circFAT1 and miR-1182 was verified by dual-luciferase reporter and RNA immunocoprecipitation (RIP) assay. Finally, Western blot assay was performed to verify the regulatory effect of circFAT1 knockdown or inhibition of miR-1182 expression on TGF-β/Smad signaling pathway. Results The expression of circFAT1 was increased in GBM tissue and cells (P＜0.05). RNase R reduced linear FAT1 expression without affecting circFAT1 (P＜0.05). Knockout of circFAT1 inhibited the proliferation, invasion and EMT of GBM cells (P＜0.05). Dual-luciferase reporter and RIP assay confirmed that circFAT1 targeting on miR-1182. The protein levels of TGFB2, p-SMAD2 and p-SMAD3 were decreased after circFAT1 knockdown, while protein expressions of TGFB2, p-SMAD2 and p-SMAD3 increased after inhibiting the expression of miR-1182 (all P＜ 0.05). Conclusion Knockout of circFAT1 can inhibit proliferation, invasion and EMT of GBM cells, and its mechanism may be related to the regulation of TGF-β/Smad signaling pathway by sponge miR-1182. [ABSTRACT FROM AUTHOR]

As a common middle-aged and elderly disease caused by metabolism, osteoporosis is mainly manifested as the formation of complications such as fractures caused by bone loss and increased brittleness. Therefore, how to delay the progression of osteoporosis and prevent the formation of its complications has become the most important concern of researchers. As a regulatory factor, microRNAs play an important role in regulating the progress of osteoporosis. MicroRNAs can delay the occurrence and progression of osteoporosis by regulating the expression of related signaling pathways. Previous studies have shown that the formation of osteoporosis is mostly related to microRNAs-related signaling pathways in the body. PI3K/Akt, MAPK, Wnt/3-catenin, TGF- B/BMP, Notch signaling pathways are related to microRNAs. By regulating the expression of these signaling pathways, the destruction of osteoblasts and the excessive absorption of osteoclasts in the body are intervened, thereby inhibiting the occurrence and development of osteoporosis. Studies have found that traditional Chinese medicine directly or indirectly promotes the formation of osteoblasts and inhibits the absorption of osteoclasts by intervening in the regulation of the above signaling pathways, thereby intervening in the formation and progression of osteoporosis. This article summarizes the research status of traditional Chinese medicine intervention in microRNAs-related signaling pathways, aiming to provide a reference for the in-depth study of the progress of traditional Chinese medicine intervention in osteoporosis. It also provides a theoretical basis and broad treatment space for the use of traditional Chinese medicine in clinical practice to reduce the formation of osteoporosis [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of the long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) on the migration, invasion, and epithelial-mesenchymal transition (EMT) of breast cancer cells and its mechanism. Methods Breast cancer tissue samples and adjacent normal tissue samples were collected from 20 patients with breast cancer, and normal human breast epithelial cell MCF-10A and breast cancer cell lines MCF-7, BT-549, MDA-MB-231, and MDA-MB-468 were cultured. RT-qPCR was used to measure the expression levels of SNHG1 and miR-641 in tissue samples and cells. BT-549 cells were divided into groups A to D and were transfected with si-NC (group A), si-SNHG1 (group B), si-SNHG1+anti-miR-641-NC (group C), and si-SNHG1+anti-miR-641 (group D), respectively. RT-qPCR was used to measure the expression levels of SNHG1 and miR-641 in cells; Transwell assay was used to observe cell invasion and migration abilities; Western blot was used to measure the expression levels of the EMT-related proteins E-cadherin, N-cadherin, and Vimentin. BT-549 cells were divided into groups E to H and were co-transfected with SNHG1-WT and miR-641 mimics (group E), SNHG1-WT and miR-NC (group F), SNHG1-MUT and miR-641 mimics (group G), and SNHG1-MUT and miR-NC (group H), respectively, and dual-luciferase reporter assay was used to determine the interaction between SNHG1 and miR-641. Results SNHG1 was highly expressed in breast cancer tissue (t=4.81,P0.05). Conclusion cSNHG1 is highly expressed in breast cancer tissue and cells, and downregulation of its expression can inhibit the migration, invasion, and EMT of breast cancer cells by targeting miR-641.

Objective To explore the effects of the hypoxic hepatoma-derived exosome miR-1260b on the M2 subtype of tumor-associated macrophages and the underlying mechanism. Methods MHCC97H (97H) cells were treated with 100 μmol/L CoCl2 for 24 h to obtain hypoxic 97H cells. THP-1 cells were treated with propylene glycol methyl ether acetate (PMA) for 24 h to derive M0 macrophages. The relative expression of CD11b in THP-1 cells was measured by real-time quantitative PCR (RT-qPCR). After co-culture with normoxic/hypoxic 97H cells for 48 h, the relative gene expression of CD163, CD206, and TNF-α in M0 macrophages was measured by RT-qPCR. The exosomes of normoxic/hypoxic 97H cells were extracted by low temperature differential centrifugation. A transmission electron microscope was used to observe the shape of the exosomes. The particle diameter was measured using a nanoparticle tracking analyzer. Western blot was used to determine the relative expression of apoptosis-inducing factor 6-interacting protein (Alix) and calnexin in the exosomes. After co-culture with the exosomes for 48 h, the relative expression of CD206 in M0 macrophages was measured by RT-qPCR. The exosomes labeled with Dil stain were co-cultured with M0 macrophages for 24 h, and then M0 macrophages were examined for the fluorescence reaction using a fluorescence microscope. The expression of miR-1260b in the exosomes was measured by RT-qPCR. After M0 and M2 macrophages were transfected with miR-1260b Mimic/Inhibitor, the expression of CD206 and TNF-α in the cells was determined by RT-qPCR. After co-culture with normoxic/hypoxic 97H cells transfected with miR-1260b Inhibitor, M0 macrophages were measured for the relative expression of CD206 and TNF-α by RT-qPCR. Results There was significantly high expression of CD11b in M0 macrophages derived from THP-1 cells after 24 h PMA treatment (t=78.14,P

Objective To investigate the expression of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) in the epithelial-mesenchymal transition (EMT) model of human bronchial epithelial cell line 16HBE induced by human transforming growth factor-β1 (TGF-β1). Methods 16HBE cells were cultured in vitro, and the experiment established control group and treatment group. The cells in the treatment group were induced by TGF-β1 to establish an EMT cell model, and those in the control group were added with an equal volume of RPMI basic culture medium. At 24, 48, and 72 h after TGF-β1 treatment, an inverted microscope was used to observe cell morphology and distribution. At the time point when the cells in the treatment group began to show obvious spindle-shaped changes, the methods of RNA separation, reverse transcription, and quantitative real-time PCR were used to measure the relative expression levels of lncRNAs and miRNAs in the two groups. Results After 48 h of TGF-β1 treatment, the cells in the treatment group showed obvious spindle-shaped changes and an increase in intercellular space, suggesting that the EMT model was successfully established. At this time point, there were significant differences between the two groups in the relative expression levels of TBILA, NKILA, LNCRNA-ATB, HOTAIR, NEAT1, miR-125b-5p, miR-21-3p, miR-21-5p, miR-27a-3p, miR-27a-5p, miR-141-3p, miR-200c-3p, miR-17-5p, miR-34a-5p(t=-16.353-6.460,P

Diabetic osteoporosis (DOP) is a common bone metabolic disease in patients with diabetes. Under the high glucose (HG) environment, abnormally expressed microRNA (miRNA) interferes with osteogenic differentiation of bone marrow mesenchymal stem cells (BM-MSCs) by regulating key molecules in the Wnt/β-catenin signaling pathway, leading to the occurrence and development of DOP. Exploring the role of miRNA in DOP can provide new ideas for the diagnosis and treatment of DOP.

Osteoporosis as a metabolic disease among the diseases of the elderly has always been regarded as a key and difficult point to study. How to delay the progression of osteoporosis has become the most important issue. MicroRNAs are key regul ators of orthopedic diseases. The changes in their expression have a regu latory effect on delaying the progression of osteoporosis. Bone-derived exosomal microRNAs may delay the occurrence and progression of osteoporosis by regulating the expression of related factors. This article reviews the correlation between bone-derived exosomal microRN As and osteoporosis, in order to provide some new therapeutic ideas for bone-derived exosomal microRNAs in the treatment of osteoporosis. [ABSTRACT FROM AUTHOR]

Metabolic reprogramming is considered to be one of the top characteristics of tumor cells. Ample experimental studies have shown that microRNAs, which are a group of multifunctional non-coding RNAs, play an important role in the development of hepatocellular carcinoma (HCC) through lipid metabolic reprogramming. The current review briefly introduces the recent progress of specific microRNAs targeting at lipid metabolic reprogramming in HCC, which may provide a potential strategy for clinical targeting tumor therapy.

BACKGROUND: Studies have found that naringin affects bone metabolism directly through Wnt, transforming growth factor β, MAPK signaling pathway, and osteoclast signaling pathway, as well as indirectly through P13K-Akt and vascular endothelial growth factor signaling pathway. Naringin can promote bone repair and retard osteoporosis. OBJECTIVE: To investigate the effect of naringin on the proliferation and osteogenic differentiation of osteoblasts by targeting the activation of connexin 43/ERK1 signaling pathway through down-regulation of miR-206. METHODS: Rat osteoblasts (ROB cells) were treated and cultured with different concentrations of naringin (1, 10, 100 mg/L and 1, 10 g/L), and the cell proliferation was detected by cell counting kit-8 assay. Naringin at 100 mg/L and 1, 10 g/L were used for subsequent experiments. Osteoblasts with nondrug culture were used as controls. RT-qPCR was used to detect the relative expression levels of miR-206, connexin 43 and ERK1 mRNAs in ROB cells to verify their targeting relationship. Western blot was used to detect the protein expression levels of ERK1/2 and P-ERK in ROB cells. Alkaline phosphatase activity and calcification ability in ROB cells were observed by alkaline phosphatase staining and alizarin red staining, respectively. RESULTS AND CONCLUSION: Naringin significantly promoted the proliferation activity of ROB cells (P < 0.05). The absorbance value and relative proliferation rate of ROB cells increased as the administration concentration of naringin increased in a certain range. When the mass concentration was 1 g/L, the cell proliferation activity was the strongest. Naringin significantly inhibited the expression of miR-206 mRNA in ROB cells and promoted the expression of connexin 43 mRNA and ERK1/2 and P-ERK protein (P < 0.05). Naringin could significantly promote the activity and expression of alkaline phosphatase and the level of cellular calcification in ROB cells (P < 0.05). Moreover, naringin at 1 g/L showed the best effect. To conclude, naringin can target and activate the connexin 43/ERK1 signaling pathway by down-regulating the expression of miR-206, thereby promoting the proliferation and osteogenic differentiation of ROB cells. [ABSTRACT FROM AUTHOR]

Objective To explore the effect of exosomal miR-1260a derived from human umbilical mesenchymal stem cells (hUC-MSCs) on apoptosis of granulosa cells (GCs) in polycystic ovary syndrome (PCOS) by targeting CASP8. Methods hUC-MSCs were obtained from the umbilical cord of healthy full-term fetus by tissue explants adherent method. The surface markers CD73 and CD90 were detected by flow cytometry. The hUC-MSCs- exosomes (exos) were extracted from the supernatant of hUC-MSCs, and the morphology was observed by transmission electron microscopy (TEM). The surface heat shock protein (HSP70) and tumor susceptibility gene 101 (TSG101) were detected by Western blot assay. Confocal microscope was used to observe whether PKH67 labeled hUC-MSCs-exos could be absorbed by GCs. Western blot assay was used to assess the protective effect of hUC-MSCs-exos on PCOS GCs. Clinical samples of GSE69909 were used for bioinformatics analysis. The differentially expressed miRNAs in hUC-MSCs-exos were obtained and verified by qPCR. miR-1260a mimics and negative control (NC) were synthesized and then transfected into KGN cells. Subsequently, cell apoptosis was measured by flow cytometry. Target genes of miR-1260a were predicted using Target Scan Human 7.2 database and verified by a dual-luciferase reporter gene assay. Expression levels of miR-1260a and CASP8 before and after uptake of hUC-MSCs-exos by PCOS GCs were detected by qPCR. Results The isolated cells accorded with the characteristics of hUC-MSCs. hUC-MSCs-exos were circular or elliptical membranous vesicle with diameter ranged from 30-150 nm and expressed the typical exosome markers HSP70 and TSG101. Confocal microscopy results showed that hUCMSCs-exos could be absorbed by GCs. Compared with the control group, the expression of Cleaved-Caspase-8, CleavedCaspase-3 and Bax were significantly down-regulated and the expression of Bcl-2 was significantly up-regulated in the hUC-MSCs supernatant treated and the hUC-MSCs-exos treated groups (P＜0.05). After GSE69909 database screening and qPCR verification, it was found that miR-1260a was enriched in hUC-MSCs-exos, and the overexpression of miR-1260a significantly inhibited the apoptosis of KGN cells (P＜0.05). A dual-luciferase reporter gene assay showed that CASP8 was a direct target of miR-1260a. Moreover, the uptake of hUC-MSCs-exos by PCOS GCs increased the expression of miR-1260a and decreased the expression of CASP8 (P＜0.05). Conclusion Our study reveals that exosomal miR-1260a derived from hUC-MSCs inhibits apoptosis of GCs in PCOS by targeting CASP8. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Clinical Healthcare is the property of Chinese Journal of Clinical Healthcare and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The vascular cambium, part of the secondary lateral meristem, contributes to the lateral growth of a plant. In recent years, many studies have strengthened our understanding of the vascular cambium. However, we still know far less about the vascular cambium than the apical meristem. Genetic and molecular studies have revealed that the proliferation and differentiation of cambium is regulated by many factors, including long-distance hormone signals, short-range peptide signals, and interactions between them. In addition, a large number of transcription factors and microRNAs also play a crucial role in the regulation of the vascular cambium activities. This review focuses on the novel discoveries on the development of vascular cambium and its regulation of proliferation and differentiation. The review also summarizes the current research and prospects for future research in this field. [ABSTRACT FROM AUTHOR]

The specific placenta-derived exosomes are important mediums for the communication between cells at the mother-to-fetus interface. During pregnancy, the placenta releases a large number of exosomes that promote the growth and development of embryos. These exosomes contain proteins, lipids, microRNAs, etc. As a kind of bioactive substances in exosomes, microRNAs participate in the occurrence and development of fetal growth restriction (FGR). Therefore, microRNAs may play an important role in the early diagnosis, clinical treatment and prognosis of diseases. In addition, the placental alkaline phosphatase (PLAP) and cell-free DNA (cfDNA) derived from exosome can also be used as specific markers in the clinical diagnosis of FGR. FGR is one of the common complications in obstetrics, which is the second leading cause of perinatal death. Therefore, early etiological diagnosis is extremely important. This article introduces the function of placenta-derived exosome and reviews its application in clinical diagnosis of FGR. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Although many studies have been carried out on the complex physiological and pathological mechanisms of spinal cord injury, there is still a lack of satisfactory treatment methods. Studies have shown that non-coding RNAs associated with secondary injuries, such as oxidative stress, inflammation, autophagy and apoptosis, are differentially expressed after spinal cord injury. Therefore, non-coding RNAs have potential as therapeutic targets after spinal cord injury. OBJECTIVE: Based on the latest research progress, to review the functional roles and regulatory mechanisms of non-coding RNAs in spinal cord injury, in order to provide new ideas for clinical treatment of spinal cord injury. METHODS: Using “spinal cord injury” AND “non-coding RNA” OR “microRNA” OR “long non-coding RNA” OR “circRNA” AND “oxidative stress” OR “inflammation” OR “autophagy” OR “apoptosis” as English and Chinese keywords, PubMed, Web of Science, CNKI and WanFang databases were searched. According to inclusion and exclusion criteria, 75 articles were reviewed. RESULTS AND CONCLUSION: After spinal cord injury, non-coding RNAs associated with secondary injury such as oxidative stress, inflammation, autophagy and apoptosis were significantly differentially expressed, resulting in differential expression of target genes and changes in cell functions. Regulating non-coding RNAs to antagonize oxidative stress, intervening microglia activation, polarization and inflammatory pathways to reduce inflammation, maintaining moderate levels of autophagy and keeping autophagy flux unobstructed, and inhibiting apoptosis may be the breakthrough points to promote the repair of spinal cord injury. [ABSTRACT FROM AUTHOR]

Exosomes are nano-sized phospholipid bilayer vesicles containing abundant and complex biomolecules, such as DNA, mRNAs, microRNAs (miRNAs), lipids, and proteins. Exosomes can be secreted and ingested by most types of cells to transfer information through intercellular transport. After uptake by recipient cells, exosomes release bioactive substances to regulate the biological processes of recipient cells, such as promoting tumor growth and metastasis. Changes of exosomes and their contents are associated with a variety of diseases. In recent years, the role of exosomal miRNAs in the development and progression of hepatocellular carcinoma (HCC) caused by viral hepatitis has attracted wide attention, and exosomal miRNAs from different sources play different roles in this process. This article briefly reviews the research on the role of exosomal miRNAs in the development and progression of viral hepatitis-related HCC and proposes that exosomal miRNAs may be the targets for immunotherapy for HCC microenvironment. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of lupeol on the proliferation, migration and invasion of non-small cell lung cancer (NSCLC) NCI-H1299 cells by regulating miR-100-5p. Methods NCI-H1299 cells cultured in vitro were divided into the normal control (NC) group (untreated), the low-dose group (12.5 µmol/L lupeol), the medium-dose group (25 µmol/L lupeol), the high-dose group (50 µmol/L lupeol), the miR-NC group (transfected with miR-NC), the miR-100- 5p group (transfected with miR-100-5p), the anti-miR-NC+high-dose group (the cells were treated with 50 µmol/L lupeol after transfected with anti-miR-NC), and the anti-miR-100-5p+high-dose group (the cells were treated with 50 µmol/L lupeol after transfected with anti-miR-100-5p). CCK-8 and colony formation assays were performed to evaluate the proliferation of NCI-H1299 cells. Transwell method was applied to detect the migration and invasion of NCI-H1299 cells. RT-qPCR was used to detect the expression of miR-100-5p. Western blot assay was used to detect the expression of CyclinD1, matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9) proteins. Results Compared with the NC group, NCI-H1299 cell viability, colony formation number, migration number, invasion number, the expression levels of CyclinD1, MMP2 and MMP9 proteins were decreased in the low, medium and high dose groups (P＜0.05), and the expression of miR-100-5p was significantly increased (P＜0.05). Compared with the miR-NC group, the expression of miR100-5p was increased, the NCI-H1299 cell viability, colony formation number, migration number, invasion number, the expression of CyclinD1, MMP2 and MMP9 proteins decreased in the miR-100-5p group (P＜0.05). Compared with the antimiR-NC+ high-dose group, the expression of miR-100-5p was decreased, NCI-H1299 cell viability, colony formation number, migration number, invasion number, the expression of CyclinD1, MMP2 and MMP9 proteins increased in the antimiR-100-5p+ high-dose group (P＜0.05). Conclusion Lupeol inhibits the proliferation, migration and invasion of NSCLC cells NCI-H1299 by up-regulating miR-100-5p. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of down-regulation of miR-106a-5p on hydrogen peroxide (H2O2)- induced cardiomyocyte damage and Janus kinase 1 (JAK1)/signal transducer and activator of transcription 3 (STAT3) pathway. Methods Different concentration gradients of H2O2 (0, 50, 100, 200 and 400 µmol/L H2O2) were used to treat rat cardiomyocytes H9c2. Rat cardiomyocytes H9c2 were divided into the control group, the H2O2 group (100 µmol/L H2O2), the miR-106a-5p NC group (100 µmol/L H2O2+ transfected with miR-106a-5p NC) and the miR-106a-5p siRNA group (100 µmol/L H2O2+ transfected with miR-106a-5p siRNA). Real-time fluorescent quantitative PCR (qPCR) method was used to detect the expression of miR-106a-5p. CCK-8 method was used to detect cell proliferation. Flow cytometry was used to detect cell apoptosis. LDH content, GSH-Px activity in cell culture fluid, MDA content and SOD activity in cells were detected. Western blotting (WB) was used to detect the expression of JAK1/STAT3 pathway related proteins in cells. Results According to the H2O2 concentration gradient experiment, 100 µmol/L H2O2 was selected for subsequent experiments. Compared with the control group, the proliferation inhibition rate, apoptosis rate, miR-106a-5p level, MDA content, p-JAK1/JAK1, p-STAT3/STAT3 protein levels in H9c2 cells and LDH content in cell culture fluid were significantly increased in the H2O2 group (P＜0.05). The GSH-Px activity in cell culture fluid and SOD activity in cells significantly reduced (P＜0.05). There were no significant differences in above indicators between the H2O2 group and the miR-106a-5p NC group (P＞0.05). Compared with the miR-106a-5p NC group, the proliferation inhibition rate, apoptosis rate, miR-106a-5p level, MDA content, p-JAK1/JAK1, p-STAT3/STAT3 protein levels in H9c2 cells and LDH content in cell culture fluid were reduced significantly in the miR-106a-5p siRNA group (P＜0.05), and the GSH-Px activity in cell culture fluid and SOD activity in cells increased significantly (P＜0.05). Conclusion Down-regulation of miR-106a-5p can inhibit the activation of JAK1/STAT3 pathway, increase the level of anti-oxidative stress and reduce H2O2-induced cardiomyocyte damage. [ABSTRACT FROM AUTHOR]

Glaucoma is an irreversible and progressive retinal neurodegenerative disease. It is the second leading cause of blindness disease in the world. The pathogenesis of glaucoma is complex. Recent studies have found that non-coding RNAs play an important role in the occurrence and development of glaucoma, including microRNA, long non-coding RNA and circular RNA, which provide promising targets and novel ideas for the diagnosis and treatment of glaucoma. This article will review the research progress of non coding RNA in glaucoma in order to provide reference for clinical science research. [ABSTRACT FROM AUTHOR]

Objective To explore the expression of miR-149-3p in heart tissues of newborn mice with congenital heart disease (CHD) and its effect on differentiation of mouse embryonic teratoma P19 cells. Methods The newborn mouse model of ventricular septal defect CHD was established. On the 19th day of pregnancy, HE staining was used to observe pathological changes of fetal heart. Then qPCR was used to detect the expression levels of miR-149-3p and heat shock protein family B in fetal mouse heart tissue member 6 (HSPB6) mRNA in heart tissue of fetal mice. Dimethyl sulfoxide (DMSO) was used to induce P19 cells to differentiate into cardiomyocytes, and cells on the 0 th, 5 th and 10 th days of differentiation were collected. qPCR was used to detect markers of myocardial differentiation GATA4, cTnT, the mRNA expression level of atrial natriuretic peptide (ANP) and HSPB6 mRNA and miR-149-3p expression levels during the induction of differentiation. P19 cells were infected with miR-149-3p overexpression lentivirus and empty lentivirus. After induction for 10 days by DMSO, the expression of cTnI protein in cells was detected by immunofluorescence staining. mRNA expression levels of myocardial differentiation markers were detected by qPCR. The dual-luciferase reporter gene experiment was used to verify the targeting relationship between miR-149-3p and HSPB6. Results Compared with the normal group, the newborn mice in the CHD group developed cardiac ventricular septal defect, with high expression of miR- 149-3p and low expression of HSPB6 in cardiac tissue (P＜0.01). During the differentiation of P19 cells into cardiomyocytes, the expression levels of GATA4, cTnT, ANP and HSPB6 mRNA were gradually increased, while the expression level of miR-149-3p was gradually decreased (P＜0.05). After 10 days of differentiation, the overexpression of miR-149-3p significantly reduced the differentiation rate of cardiomyocytes, and down-regulated the mRNA expression levels of GATA4, cTnT and ANP (P＜0.01). The dual luciferase reporter gene experiment confirmed that miR-149-3p could target the expression of HSPB6. Conclusion miR-149-3p might inhibit the differentiation of P19 cells in to cardiomyocytes through targeted down- regulation of HSPB6 [ABSTRACT FROM AUTHOR]

Chronic endometritis (CE), a persistent endometrial inflammation caused by pathogen infection, is related to adverse pregnancy outcomes. However, there are still disagreement in the diagnosis and treatment of CE. Exploring the inflammatory mechanism of CE is helpful to improve the diagnosis and treatment of CE. The occurrence and development of CE is closely related to the activation of inflammatory pathways, such as TLR and NLR pathways. The metabolic changes of endometrial immune cells, dysregulation of microRNAs and alteration of DNA methylation patterns can abnormally regulate the generation of inflammatory mediators that are related to the pathogenesis and development of CE. The inflammatory mechanism of CE was reviewed in this article, providing a valuable information for understanding in-depth the pathogenesis and pathophysiological changes of CE, and for seeking more standardized and effective diagnostic and treatment measures of CE. [ABSTRACT FROM AUTHOR]

Objective　To explore the effect of hsa-miR-130b-3p on the reprogramming of human dental iPSCs. Methods　LV3 （H1/GFP&Puro）-hsa-miR-130b-3p-mimics plasmid was designed and synthesized. The plasmid was transduced into human DPSCs by Lipofectamine 3000 kit according to the manufacturer’s instructions. Fluorescence microscopy was used to observe the cells and transfection efficiency was verified by RT-qPCR. Sendai reprogramming kit was used to induce two groups of DPSCs （miR-130b-3p-DPSCs in the experimental group and DPSCs in the control group） into iPSCs. The morphology and reprogramming efficiency were compared and the expression of Oct4/Nanog/KOS/Klf4/c-Myc was detected by RT-PCR in two groups of iPSCs. Results　hsa-miR- 130b-3p overexpression plasmid was significantly expressed in DPSCs 48h after transfection， indicating high transfection efficiency （P < 0.01）. The two groups of iPSCs obtained by Sev reprogramming showed flat and dense round clones with clear and smooth edges，uniform cell morphology and large nucleolus in the colonies. RT-PCR results showed that cells in both groups could express the specific markers of stem cells Oct4 and Nanog. At the same time，exogenous virus SeV or transcription factors KOS/Klf4/c-Myc were no longer expressed. RT-PCR showed that cells in both groups all expressed specific markers Oct4 and Nanog， while SeV or KOS/Klf4/ C-MYC were not detected. The reprogramming efficiency of the experimental group was higher than that of the control group （0.037% and 0.018% respectively，P < 0.05）. Conclusion　hsa-miR-130b-3p could promote the reprogramming efficiency of human DPSCs. Our research provides theoretical foundation for dental iPSCs application in dental pulp regenerative therapy. [ABSTRACT FROM AUTHOR]

Objective To investigate the influence of long non-coding RNA (lncRNA) OPA-interacting protein 5 antisense transcript 1 (OIP5-AS1) on the proliferation, apoptosis, migration and invasion of glioma cells. Methods Tissue specimens from 33 glioma patients (14 low-grade gliomas and 19 high-grade gliomas) and 33 patients with craniocerebral injury were collected. Real-time quantitative PCR (qPCR) was used to detect the mRNA expression levels of OIP5-AS1, microRNA-942-5p (miR-942-5p) and checkpoint kinase 1 (CHEK1) in tissue samples and cells, and analyze the correlation between OIP5-AS1, miR-942-5p and CHEK1 mRNA expression level in glioma tissues. Human glioma cell lines U87, SHG-44, U251 and H4 and normal human astrocytes NHA were cultured in vitro. The expression of CHEK1 protein in cells were detected by Western blot assay. U87 cells were divided into the control (NC) group, the siRNA negative control (si-NC) group, the OIP5-AS1 siRNA (si-OIP5-AS1) group, the si-OIP5-AS1+inhibitor negative control (si-OIP5- AS1+anti-NC) group and the si-OIP5-AS1+miR-942-5p inhibitor (si-OIP5-AS1+anti-miR-942-5p) group. Cells were transfected with Lipofectamine 3000 reagent. After transfection, the expression levels of OIP5-AS1, miR-942-5p and CHEK1 mRNA and protein in cells were detected by qPCR and Western blot assay. MTT assay was used to detect the cell proliferation activity. Flow cytometry was used to detect cell apoptosis. Transwell assay was used to detect cell migration and invasion abilities. Finally, the interaction of OIP5-AS1 and miR-942-5p and CHEK1 and miR-942-5p were verified by dual luciferase and RNA immunoprecipitation (RIP) experiments. Results OIP5-AS1 and CHEK1 were overexpressed in glioma tissue and cells, while miR-942-5p was underexpressed (all P＜0.05). Correlation analysis showed that OIP5-AS1 was negatively correlated with miR-942-5p, and miR-942-5p and CHEK1 mRNA was negatively correlated in glioma tissue. The expression level of CHEK1 mRNA was positively correlated with OIP5-AS1. The expression levels of OIP5-AS1 and CHEK1 mRNA were significantly higher in high-grade glioma tissue than those in low-grade glioma tissue, while the expression level of miR-942-5p was significantly lower in high-grade glioma tissue than that in low-grade glioma tissue (P＜0.01). Silencing OIP5-AS1 significantly up-regulated miR-942-5p and inhibited the mRNA and protein expression of CHEK1 (P＜0.05). Silencing OIP5-AS1 significantly inhibited the proliferation, migration and invasion of U87 cells, promoting apoptosis of U87 cells (P＜0.05). Down-regulation of miR-942-5p could up-regulate the expression of CHEK1 and block the effects of OIP5-AS1 silencing on glioma cell proliferation, migration, invasion and apoptosis (P＜0.05). Dualluciferase and RIP experiments confirmed that miR-942-5p was a target of OIP5-AS1, and CHEK1 was a downstream target gene of miR-942-5p. Conclusion Silencing OIP5-AS1 may inhibit the expression of CHEK1 by up-regulating miR-942- 5p, inhibit the invasion and migration of glioma cells, and promote cell apoptosis. [ABSTRACT FROM AUTHOR]

Objective To screen hub genes and miRNA interaction in aging osteoporosis. Methods The GSE35956 gene chip data set was downloaded from GEO database, and the differentially expressed genes (Degs) in bone marrow mesenchymal stem cells were screened by R language in patients with osteoporosis. GO enrichment and KEGG pathway were analyzed in Degs using DAVID database. String database and Cytoscape software were used to analyze the protein interaction network and screen hub genes. The mirnas interacting with hub genes were predicted by Targetscan database, and the predicted mirnas were enriched by funrich database. Bone marrow mesenchymal stem cells from 3 to 4 month-old (the young group) and 18 to 20 month-old (the old group) in C57BL/6 mice were extracted and cultured. The expression levels of miRNA in bone marrow mesenchymal stem cells were verified by qPCR technique in the young and the old groups. Results A total of 982 up-regulated Degs and 99 down-regulated degs were identified in patients with osteoporosis. Degs were mainly enriched in plasma membrane adhesion molecule-mediated homologous cell adhesion and calcium ion binding, and were mainly involved in neuroactive ligand-receptor interaction signaling pathways. PPI interaction network analysis identified eight core genes: leptin (LEP), lymphocyte-specific protein tyrosine kinase (LCK), WT1 transcription factor (WT1), SRY-box transcription factor 10 (SOX10), integrin subunit beta 2 (ITGB2), albumin (ALB), cholecystokinin (CCK) and bone morphogenetic protein 7（BMP7). The interaction between 105 miRNA and 6 core genes was predicted by Trargetscan qPCR results showed that BMP7, CCK, ITGB2 and SOX10 genes in bone marrow mesenchymal stem cells were significantly up regulated in the old group compared with those of the young group. It is consistent with the results of bioinformatics analysis. Conclusion The expression levels of the selected core genes are related to the differentiation degree of bone marrow mesenchymal stem cells in aged mice. The identified miRNA may be a diagnostic marker and a therapeutic target for aging osteoporosis [ABSTRACT FROM AUTHOR]