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Objective To investigate the effects of thrombospondin1 (THBS1) gene knockout on immune microenvironment and tumor progression of colorectal cancer. Methods THBS1 gene knockout (THBS1-/-) mice were constructed and its genotypes were determined by PCR and agarose gel electrophoresis. Subcutaneous tumor bearing and intraperitoneal implantation metastasis models of colorectal cancer were constructed in wild type (WT) and THBS1-/- mice to observe the effect of THBS1 on tumor growth. Immune cells in epididymal adipose of tumor bearing mice of both types were detected by flow cytometry. Results Compared with the WT mice, THBS1-/- mice showed no difference in tumor growth in colorectal cancer subcutaneous tumor bearing model (P>0.05), but significantly inhibited tumor growth in intraperitoneal implantation metastasis model (P < 0.05). Subsequently, flow cytometry indicated that the proportion of total macrophages in the epididymal adipose tissue was increased in the THBS1-/- mice than the WT mice (P < 0.01), with the proportion of M1-like macrophages (typical or proinflammatory type) increased (P < 0.01) and that of M2-like macrophages (alternately activated or anti-inflammatory type) decreased (P < 0.01). The proportion of myeloid-derived suppressor cells (MDSC) was decreased (P < 0.05), that of Ly6C subgroup was increased (P < 0.01), that of Ly6G subgroup was decreased (P < 0.05), that of CD8+ T cells was significantly increased (P < 0.01), and that of CD4+ T cells was decreased (P < 0.01). There were no changes in the proportions of total macrophages, M1-like macrophages and M2-like macrophages in the peripheral blood of intraperitoneal implantation metastasis model mice (P>0.05). The proportions of MDSC and ly6C subgroup were not changed (P>0.05), while that of ly6G subgroup were decreased (P < 0.05). The proportion of CD8+ T cells was significantly decreased (P < 0.05), while that of CD4+ T cells was not changed (P>0.05). Conclusion THBS1 gene knockout inhibits the intraperitoneal metastasis of colorectal cancer cells by enhancing tumor immunity.

Objective To investigate the effect of thrombospondin-1(TSP-1) knockout on radiation-induced pulmonary fibrosis and explore its underlying mechanism. Methods Male wild type C57BL/6 mice (6~8 weeks old, WT mice) and TSP-1 knockout mice (TSP-1-/- mice) were subjected and received 16 Gy 60Co γ-ray whole lung irradiation (IR) to induce radiation pulmonary fibrosis, and then, the mice were assigned into WT+IR group and TSP-1-/-+IR group, respectively, with 6 mice in each group.In 16 weeks after irradiation, HE staining was performed to observe the morphological changes in lung tissues, and Sirius red staining was used to observe the collagen expression in lung tissues.qRT-PCR was employed to detect the mRNA expression of TGF-β1 and Collagen Ⅰ in lung tissues.Micro-CT scanning was adopted to evaluate lung injury and substantial lung changes.FlexiVent system was employed to assess pulmonary function.Immunofluorescence staining was conducted to measure the protein levels of LC-3 and p62 in lung tissues.Transmission electron microscopy (TEM) was used to observe the cellular autophagic vesicles in lung tissues. Results Compared with the WT+IR group, the TSP-1-/-+IR group had reduced lung injury and collagen deposition in lung tissue, significantly lower mRNA levels of TGF-β1 and Collagen Ⅰ in lung tissue (P < 0.01), and improved pulmonary function.Immunofluorescence assay and TEM showed that autophagy was observed in the mice of TSP-1-/-+IR group. Conclusion TSP-1 knockout can alleviate radiation-induced pulmonary fibrosis, which may be related to activation of autophagy.

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.)

To investigate the relationship between serum amyloid A (SAA), thrombospondin-1 (TSP-1), folic acid (FA) and unexplained recurrent spontaneous abortion (URSA), and to analyze the value of combined detection of SAA, TSP-1, FA in predicting URSA. 80 URSA patients (URSA group) who were admitted to the department of Obstetrics and Gynecology of our hospital from January 2019 to January 2021 and 102 normal pregnant women (control group) during the same period were selected. Serum SAA, TSP-1 and FA levels were detected, and clinical data were collected. Multivariate Logistic regression was used to analyze the influencing factors of URSA, and receiver operating characteristic curve (ROC) was used to analyze the predictive value of serum SAA, TSP-1 and FA on the occurrence of URSA. Serum SAA and TSP-1 in URSA group were higher than those in control group (P<0.05), FA level was lower than that in control group (P<0.05). In URSA group, the proportion of age ≥ 35 years old, smoking history, drinking history, junior high school education and reproductive tract infection were higher than those in control group (P<0.05). There were no significant differences in body mass index, URSA family genetic history and occupation between the two groups (P>0.05). Multivariate Logistic regression analysis results show that:Smoking, drinking, reproductive tract infection, SAA and TSP-1 were risk factors for URSA (P<0.05), FA was a protective factor for URSA (P<0.05). ROC curve analysis results show that: the area under the curve predicted by SAA, TSP-1 and FA was 0.744, 0.719 and 0.670, and the area under the curve predicted by SAA, TSP-1 and FA was 0.872, which was higher than that predicted by alone (P<0.05). The serum levels of SAA and TSP-1 in URSA patients are increased, while FA is decreased, which is related to the occurrence of URSA. The combination of SAA, TSP-1 and FA has certain value in the prediction of URSA. [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.)

This study aimed to investigate the role of macrophage polarization in the treatment of liver fibrosis by Fuzheng Huayu Tablets(FZHY) through single-cell, transcriptome sequencing and in vitro and in vivo experiments. Liver fibrosis-related datasets, transcriptomic datasets, and single-cell sequencing datasets were obtained from the Gene Expression Omnibus(GEO) database to screen differential genes. Liver fibrosis-related genes were obtained from GeneCards, DisGeNET, NCBI, PharmgKB, TTD and OMIM databases. Macrophage polarization-related genes were obtained from the GeneCards database. The above three gene sets were intersected to construct a protein-protein interaction(PPI) network. Cytoscape software was used to screen core proteins, and the expression pattern of core proteins was visualized by single-cell sequencing. A mouse model of liver fibrosis was constructed using carbon tetrachloride(CCl&#95;4). Hematoxylin-eosin(HE) staining and Masson staining were used to observe the pathological morphology of liver tissues. The expressions of α-smooth muscle actin(α-SMA) and transforming growth factor-β1(TGF-β1) were detected by immunohistochemistry. The levels of alanine aminotransferase(ALT) and aspartate aminotransferase(AST) were detected by colorimetry. The le-vels of inflammatory factors in serum were detected by the enzyme-linked immunosorbent assay(ELISA). Furthermore, the expressions of α-SMA, TGF-β1, cluster of differentiation 86(CD86) and thrombospondin 1(THBS1) in liver tissues were detected by Western blot(WB). Lipopolysaccharide(LPS) was used to stimulate RAW264.7 cells to construct the M1 macrophage polarization model. The cell counting kit-8(CCK-8) method was used to detect cell viability. WB was used to detect the protein expressions of CD86 and THBS1 in cells, and the messenger ribonucleic acid(mRNA) expression levels of tumor necrosis factor-α(TNF-α) and interleukin(IL)-1β by real-time fluorescent quantitative reverse transcription polymerase chain reaction(RT-qPCR). The results showed that a total of 26 potential genes related to the polarization of liver fibrosis macrophages were obtained, and 10 core proteins related to the polarization of liver fibrosis macrophages such as THBS1, lumican(LUM) and fibulin-5(FBLN5) were screened. Single-cell data analysis indicated that THBS1, ranking highest, may be expressed by M1 macrophages. Animal experiments demonstrated that FZHY reduced inflammatory cell infiltration and collagen deposition in CCl&#95;4-induced mouse liver, relieved liver injury and inflammation levels, and inhibited the expressions of α-SMA, TGF-β1, CD86, and THBS1 proteins. Cell experiments revealed that FZHY significantly reduced intracellular expression of CD86 and THBS1 proteins and mRNA levels of TNF-α and IL-1β. In conclusion, FZHY may ameliorate liver fibrosis by inhibiting THBS1 protein expression, suppressing M1 macrophage polarization, and reducing inflammation.

Objective To investigate the expressions and significance of cathepsin S (Cat S) and thrombospondin- 1 (TSP-1) in patients with acute cerebral infarction. Methods 76 cases of acute cerebral infarction in our hospital from October 2016 to September 2017 were selected as observation group, and 68 cases of healthy physical examiners in the same period were selected as control group. All subjects were tested for total cholesterol (TC), triacylglycerol (TG), low density lipoprotein (LDL), high density lipoprotein (HDL) levels, and carotid intima media thickness (IMT) Enzyme linked immunosorbent assay (ELISA) was used to detect the levels of Cat S and TSP-1 in serum, Pearson method was used to analyze the relationships between Cat S and TSP-1 with their correlation with blood lipid and carotid artery IMT, and receiver operating characteristic (ROC) curve was used to evaluate the diagnostic efficiency of Cat S and TSP-1 in acute cerebral infarction. Results The levels of TC, TG and LDL in the observation group were significantly higher than those in the control group, and HDL was significantly lower than that in the control group (P<0.05); serum Cat S and TSP-1 levels in the observation group were significantly higher than those in the control group (P<0.05); there was a significant positive correlation between Cat S with TSP-1 (P<0.05) ; Cat S and TSP-1 were positively correlated with TC, TG, LDL and carotid IMT respectively, and were negatively correlated with HDL (P<0.05); ROC showed that the diagnostic value of Cat S was significantly higher than that of TSP-1, Cat S was truncated by 69.48 pg/mL, and its sensitivity, specificity and Jorden index was 82.4%, 86.4% and 0.688, respectively; the cut-off value of TSP-1 was 266.4 ng/mL, and its sensitivity, specificity and Jorden index was 94.1%, 64.4% and 0.585 respectively. Conclusion The levels of serum Cat S and TSP-1 are increased significantly in patients with acute cerebral infarction, and they play important roles in the process of atherosclerosis. The diagnostic efficiency of Cat S is stronger than that of TSP-1,clinical detection of Cat S and TSP-1 levels is helpful for early diagnosis of acute cerebral infarction. [ABSTRACT FROM AUTHOR]

Copyright of West China Journal of Stomatology is the property of Sichuan University, West China College of Stomatology 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 expression of a disintegrin and metalloprotease with thrombospondin motifs-1 (ADAMTS-1) and its impacts on the ventricular remodeling in rats with alcoholic cardiomyopathy (ACM). Methods: Fifty healthy Wistar rats were randomly divided into the control group (n=20) and the ACM group (n=30). Rats in the ACM group were given 10% alcohol ad libitum as the drinking water and 60% alcohol (5 mL'kg'1 once per day) by intragastric administration in the first week; 10% alcohol ad libitum as the drinking water and 60% alcohol (10 mL'kg'1 twice per day) by intragastric administration in the second week; 20% alcohol ad libitum as the drinking water and 60% alcohol (15 mL • kg'1 twice per day) by intragastric administration from week 3 to week 16; and 30% alcohol ad libitum as the drinking water and 60% alcohol (15 rnL'kg'1 twice per day) by intragastric administration from week 17 to month 6. Animals in the control group received purified drinking water in the same regimen with alcohol treatment. Before and 6 months after initiating the study, left ventricular end diastolic diameter (LVEDD), left ventricular ejection fraction (LVEF), and fractional shortening (FS) were assessed by echocardiography. Histopathology of myocardium was examined with light microscopy; collagen volume fraction (CVF) and apoptotic index were analyzed by Masson staining and TUNEL assay, respectively; and protein expressions of ADAMTS-1 and syndecan-4 were analyzed using immunohistochemistry. Results: Following 6 months of alcohol feeding, compared with the control group, the LVEF and FS overtly reduced in the ACM group {P<0.01 for LVEF and P<0.05 for FS), whereas LVEDD was increased ( P<0.05). In the ACM group, the cardiomyocyte hypertrophy, disorganized cellular arrangement, adipose degeneration, myocardial fiber fracture and myolysis, interstitial vascular dilatation and congestion, extracellular space widening, fibrous proliferation, and inflammatory cell infiltration were observed by light microscopy. In addition, the CVF and apoptotic index were increased dramatically {P<0.01 for both). The protein levels of ADAMTS-1 and Syndecan-4 were higher in the ACM group than those in the control group {P<0.05 for both). Conclusions: ADAMTS-1 is over-expressed in ACM and may mediate the ventricular remodeling by degrading Syndecan-4, including ECM remodeling, myocardial fibrosis and apoptosis. [ABSTRACT FROM AUTHOR]

Objective: To investigate the dynamic expression of cluster of differentiation 47 (CD47) and its ligands signaling regulatory protein α (SIRPα) and thrombospondin-1 (TSP-1) in mice infected with Toxoplasma gondii in the second and third trimesters., Methods: C57BL/6J mice (6 to 8 weeks old) were used for modeling T. gondii infection in the first trimester, and the pregnant mice were randomly divided into the normal control and infection groups, of 10 mice in each group. Pregnant mice in the infection group were intraperitoneally injected with 150 T. gondii tachyzoites on gestational day (Gd) 6.5, while pregnant mice in the normal control group were intraperitoneally injected with the same volume of physiological saline at the same time. The uterine and placental specimens were collected from all pregnant mice on Gd12.5 and Gd18.5, and the pregnant outcomes were recorded. The pathological damages of mouse uterine and placental specimens were observed using hematoxylin-eosin (HE) staining on Gd12.5 and Gd18.5. The relative expression of CD47 , SIRPα , TSP-1 , surface antigen 1 ( SAG1 ), interferon-γ ( IFN-γ ), interleukin-2 ( IL-2 ), IL-4 and IL-13 mRNA was quantified in mouse uterine and placental specimens using real-time fluorescence quantitative PCR (qPCR) assay, and the CD47, SIRPα, TSP-1 expression was determined in mouse uterine and placental specimens using immunohistochemical staining., Results: As compared with those in the normal control group, the pregnant mice in the infection group showed back arching, bristling, trembling and listlessness during pregnancy, and several mice presented virginal bleeding and abortion. Pathological examinations showed inflammatory cell infiltration, congestion and necrosis in uterine and placental specimens of pregnant mice in the infection group, a higher abortion rate of pregnant mice was seen in the infection group than in the normal control group on Gd12.5 (χ 2 = 20.405, P < 0.001) and Gd18.5 (χ 2 = 28.644, P < 0.001). qPCR assay showed significant differences in the expression of CD47 , SIRP α, TSP-1 , SAG1 , INF-γ , IL-2 , IL-4 and IL-13 genes in mouse placental specimens between the normal control and infection groups on Gd12.5 and Gd18.5 [ F ' ( F ) = 37.511, 29.337, 97.343, 53.755, 67.188, 21.145, 8.658 and 13.930, all P values < 0.001]. Higher CD47 , SIRP α and TSP-1 gene expression was quantified in mouse placental specimens in the infection group than in the normal control group on Gd12.5 (all P values < 0.01), and lower CD47 , SIRPα and TSP-1 gene expression was quantified in the infection group than in the normal control group on Gd18.5 (all P values < 0.001), while higher SAG1 gene expression was detected in placental specimens of pregnant mice in the infection group than in the normal control group on Gd12.5 and Gd18.5 (both P values < 0.01). In addition, higher INF-γ and IL-2 expression and lower IL-4 and IL-13 expression was detected in mouse placental specimens in the infection group than in the normal control group on Gd12.5 and Gd18.5 (all P values < 0.001), and there were significant differences in the CD47 , SIRP α, TSP-1 , SAG1 , INF-γ , IL-2 , IL-4 and IL-13 gene expression in uterine specimens of pregnant mice between the normal control and infection groups on Gd12.5 and Gd18.5 [ H ( F ' and F ) = 14.951, 25.977, 18.711, 48.595, 39.318, 14.248 and 15.468, all P values < 0.01], and higher CD47 and TSP-1 expression was detected in mouse uterine specimens in the infection group than in the control group on Gd12.5 and Gd18.5 (all P values < 0.01); however, no significant difference was found in the SIRP α expression ( P > 0.05). Higher SAG1 expression was detected in uterine specimens of pregnant mice in the infection group than in the normal control group on Gd12.5 and Gd18.5 (both P values < 0.01), and higher INF -γ and IL-2 gene expression and lower IL-4 and IL-13 gene expression was found in the placental specimens of pregnant mice in the infection group than in the normal control group on Gd12.5 and Gd18.5 (all P values < 0.001). Spearman correlation analysis showed that the CD47 gene expression correlated positively with IFN-γ ( r s = 0.735, P < 0.05) and IL-2 ( r s = 0.655, P < 0.05) and negatively with IL-4 ( r s = -0.689, P < 0.05) and IL-13 expression ( r s = -0.795, P < 0.05) in the placental specimens of pregnant mice in the infection group on Gd12.5, and the CD47 gene expression correlated negatively with IFN -γ ( r s = -0.745, P < 0.05) and IL-2 expression ( r s = -0.816, P < 0.05) and positively with IL-4 ( r s = 0.704, P < 0.05) and IL-13 ( r s = 0.802, P < 0.05) in the placental specimens of pregnant mice in the infection group on Gd18.5. Immunohistochemical staining showed mild CD47, SIRPα and TSP-1 expression in uterine and placental specimens of pregnant mice in the normal control group on Gd12.5 and Gd18.5, strong CD47, SIRPα and TSP-1 expression in the placental specimens of pregnant mice in the infection group on Gd12.5 and strong CD47 and TSP-1 expression in the uterine specimens of pregnant mice in the infection group on Gd12.5., Conclusions: T. gondii infection in the first trimester may cause abnormal expression of CD47 and its ligands SIRPα and TSP-1 in the maternal-fetal interface of pregnant mice in the second and third trimesters, which may be associated with the immune escape of T. gondii at the maternal-fetal interface.

Objective: To investigate the effect of thrombospondin-1 (TSP-1) on apoptosis of human megakaryocytic leukemia cell line Meg-01 and its possible mechanism., Methods: The expression of CD36 antigen in Meg-01 cells was detected by flow cytometry and immunocytochemistry. Meg-01 cells were cultured for 48 hours with TSP-1 and CD36 antibody FA6-152 at different concentrations. The early apoptosis and activity of caspase-3 were detected by flow cytometry. The effect of TSP-1 on the growth and differentiation of megakaryocytes was investigated by cell counting and CFU-MK culture., Results: The flow cytometry and immunocytochemistry showed that CD36 antigen was expressed on the surface of Meg-01 cells. TSP-1 (5 μg/ml) inhibited the growth of Meg-01 cells, but had unobvious effect on M-07e cells. After addition of CD36 antibody FA6-152 (5, 10, and 25 μg/ml), the inhibition effect of TSP-1 was significantly reduced. TSP-1 (2.5, 5, and 7.5 μg/ml) increased the positive expression of Annexin V (P<0.01) and caspase-3 activity (P<0.01), which indicated that TSP-1 had a significant effect on inducing apoptosis. After addition of CD36 antibody FA6-152 (25 μg/ml), the apoptosis induced by TSP-1 in Meg-01 cells was significantly reduced. TSP-1 (5, 10, and 25 μg/ml) could significantly inhibit the formation of CFU-MK in mouse bone marrow cells, while β-TG could not. CD36 antibody FA6-152 (25 μg/ml) could significantly reduce the inhibition of TSP-1 on CFU-MK., Conclusion: TSP-1 may induce apoptosis of megakaryocytic leukemia cell line Meg-01 cells via CD36/caspase-3, which provides a potential new drug development and treatment target for clinical treatment of megakaryocytic leukemia.

Objective: To explore the changes of Ⅻ antithrombin (FⅫa-AT), thrombospondin-1 (TSP-1), and lupus anticoagulant (LA) ratio in the peripheral blood factor of patients with systemic lupus erythematosus (SLE) and the clinical value of combined diagnosis of thrombotic events., Methods: A total of 133 SLE patients treated in Xingtai People's Hospital were selected and divided into simple SLE group (105 cases) and SLE complicated with thrombosis group (28 cases) according to whether thrombotic events occurred, and 102 cases of healthy people in the same period were selected as control. The clinical data of the 3 groups, the level of peripheral blood FⅫa-AT, TSP-1, and LA ratio were compared, the relationship between each peripheral blood index and SLE disease activity index (SLEDAI) score were analyzed. The influencing factors of thrombotic events in SLE patients were analyzed, and the value of each peripheral blood index in the diagnosis of SLE complicated with thrombotic events were evaluated., Results: The proportion of the patients with age ≥60 year, hypertension, and smoking history in SLE complicated with thrombosis group was higher than those in simple SLE group and control group (P＜0.05). The SLEDAI score, peripheral blood FⅫa-AT, TSP-1, LA ratio levels of the patients in SLE complicated with thrombosis group were significantly higher than those in simple SLE group and control group, and the simple SLE group was significantly higher than the control group (P＜0.05). FⅫa-AT, TSP-1, LA ratio in peripheral blood of SLE patients were positively correlated with SLEDAI score (r=0.663, 0.578 and 0.625). Age, blood pressure, smoking history, peripheral blood FⅫa-AT, TSP-1, LA ratio were the important influencing factors of thrombotic events in SLE patients (P＜0.05). The AUC diagnosed by the FⅫa-AT, TSP-1, and LA ratio in peripheral blood was 0.881, the 95% CI was 0.813-0.931, the sensitivity was 82.14%, and the specificity was 91.43%, which was superior to each index alone (P＜0.05)., Conclusion: Peripheral blood FⅫa-AT, TSP-1, LA ratio level changes in SLE patients are significantly related to disease activity, and the combined diagnosis of thrombotic events is more reliable.

Objective: To investigate the effects of plasma lipopolysaccharide (LPS) concentration changes on platelet release of vascular endothelial growth factor (VEGF) and thrombospondin (TSP)-1 in patients with decompensated cirrhotic portal hypertension after transjugular intrahepatic portosystemic shunt (TIPS) procedure. Methods: 169 cases with cirrhotic portal hypertension were enrolled, of which 81 cases received TIPS treatment. LPS, VEGF, and TSP-1 concentrations with different Child-Pugh class in peripheral blood plasma of patients were measured. After pre-incubation of normal human platelets with different concentrations of LPS and stimulated by collagen in vitro, platelet PAC-1 expression rate, VEGF, and TSP-1 concentrations were detected. PAC-1 expression rate and the concentrations of LPS, VEGF and TSP-1 in peripheral blood plasma of patients before and after TIPS procedure were detected. The relationship between plasma LPS, VEGF and TSP-1 concentrations and Child-Pugh score changes in patients after TIPS procedure was analyzed. Statistical analysis was performed by t-test, one-way ANOVA or Pearson's rho according to different data. Results: Plasma LPS and TSP-1 concentrations were significantly higher in Child-Pugh class C patients than class A and B, but the concentration of plasma VEGF was significantly lower than class A and B ( P < 0.01). In vitro experiments showed that concentration of LPS, TSP-1, and platelet PAC-1 expression rate was higher in the supernatant, but the difference in the concentration of VEGF in the supernatant was not statistically significant. Portal vein pressure and platelet activation were significantly decreased ( P < 0.01) in patients after TIPS procedure. Portal venous pressure, platelet activation, plasma LPS, and TSP-1 levels were significantly decreased continuously, while VEGF levels were significantly increased continuously after TIPS procedure. Plasma LPS concentration was positively correlated with TSP-1 concentration ( r = 0.506, P < 0.001), and negatively correlated with VEGF concentration ( r = -0.167, P = 0.010). Child-Pugh score change range was negatively correlated with change range of plasma VEGF concentration ( r = -0.297, P = 0.016), and positively correlated with change range of plasma TSP-1 concentration ( r = 0.145, P = 0.031) after TIPS. Conclusion: Portal venous pressure gradient, plasma LPS concentration and corresponding platelet activation was decreased in cirrhotic portal hypertension after TIPS procedure, and with TSP-1 reduction and VEGF elevation it is possible to reduce the liver function injury caused by portal venous shunt.

Objective: To investigate serum levels of von Willebrand factor lytic protease (ADAMTS13) and thrombospondin-1 (TSP1) in patients with different types of acute coronary syndrome (ACS) and their correlation with the patients' clinical prognosis., Objective: According to their disease history, results of angiography and clinical biochemical tests, a total of 405 patients undergoing coronary angiography, were divided into unstable angina (UAP) group ( n =215), acute myocardial infarction (AMI) group ( n =96), and angiographically normal group ( n =94). Serum ADAMTS13 and TSP1 levels were detected in all the patients, who were followed up for 15 months to evaluate the occurrence of long-term major cardiac adverse events (MACE)., Objective: Serum ADAMTS13 level was significantly lower and TSP1 level was significantly higher in AMI group and UAP group than in the normal group ( P < 0.001). Serum ADAMTS13 and TSP1 levels were negative correlated in ACS patients ( R =-0.577, P < 0.001). The patients experiencing MACE had significantly different serum TSP1 level from those without MACE ( P < 0.05). Cox proportion regression model analysis showed that TSP1 was a risk factor affecting the occurrence of MACE in ACS patients; Kaplan-Meier survival analysis showed that the patients with high levels of TSP1 had a higher incidence of longterm MACE than those with low TSP1 levels., Objective: A lowered serum ADAMTS13 level and an elevated TSP1 level can support the diagnosis of ACS. An elevated TSP1 level may serve as an indicator for predicting the risk of MACE in patients with ACS.

Objective: To investigate the expression and effect of microRNA-205 (miR-205) in human hypertrophic scar. Methods: The experimental research method was applied. From October 2019 to January 2020, hypertrophic scar tissue from 6 patients with hypertrophic scar (1 male and 5 females, aged (36±7) years) and remaining normal skin tissue from 6 trauma patients (2 males and 4 females, aged (38±9) years) after flap transplantation operation were collected. The above-mentioned 12 patients were admitted to the General Hospital of Northern Theater Command and met the inclusion criteria. Real-time fluorescent quantitative reverse transcription polymerase chain reaction was used to detect the mRNA expressions of miR-205 and thrombospondin-1 (TSP-1). The hypertrophic scar tissue was taken to culture the 3rd to 5th passage of fibroblasts (Fbs) for the follow-up experiments. Two batches of hypertrophic scar Fbs were divided into TSP-1+ miR-205 control group, TSP-1+ miR-205 mimic group, and TSP-1 mutant+ miR-205 control group, TSP-1 mutant+ miR-205 mimic group, which were transfected with the corresponding sequences. At 48 h after transfection, the expressions of luciferase and renal luciferase were detected by luciferase reporter gene detection kit, and the luciferase/renal luciferase ratio was calculated to indicate the activity of TSP-1. Two batches of hypertrophic scar Fbs were collected and divided into miR-205 control group, miR-205 mimic group, and miR-205 inhibitor group and miR-205 control group, miR-205 mimic group, and miR-205 mimic+ TSP-1 group, respectively, which were transfected with the corresponding sequences. At 0 (immediately), 12, 24, 36, and 48 h after transfection, the cell viability was detected by microplate reader. Two batches of hypertrophic scar Fbs were grouped and treated as described in the cell viability detecting experiment. At 24 h after transfection, Hoechst 33258 staining was performed to observe the nuclear shrinkage, so as to reflect the apoptosis of Fbs. The number of samples in cell experiment was three. Data were statistically analyzed with analysis of variance for factorial design, one-way analysis of variance, t test, and chi-square test. Results: The mRNA expression of miR-205 in hypertrophic scar tissue was 0.54±0.05, which was significantly lower than 1.26±0.07 in normal skin tissue ( t =8.213, P <0.01). The expression of TSP-1 mRNA in hypertrophic scar tissue was 1.46±0.07, which was significantly higher than 0.68±0.11 in normal skin tissue ( t =6.031, P <0.01). At 48 h after transfection, the luciferase/renal luciferase ratio reflecting the TSP-1 activity of cells in TSP-1+ miR-205 mimic group was 0.532±0.028, which was significantly lower than 0.998±0.012 in TSP-1+ miR-205 control group ( t =26.500, P <0.01), and the luciferase/renal luciferase ratio of cells in TSP-1 mutant+ miR-205 mimic group was 0.963±0.012, which was close to 0.976±0.010 in TSP-1 mutant+ miR-205 control group ( t =0.816, P >0.05). At 12, 24, 36, and 48 h after transfection, the cell viability in miR-205 mimic group was significantly lower than that in miR-205 control group ( t =6.169, 12.670, 27.130, 12.670, P <0.05 or P <0.01). At 0, 12, 24, 36, and 48 h after transfection, the cell viability in miR-205 inhibitor group was significantly higher than that in miR-205 control group ( t =6.169, 7.221, 7.787, 7.835, 13.030, P <0.05 or P <0.01). At 12, 24, 36, and 48 h after transfection, the cell viability in miR-205 mimic group was significantly lower than that in miR-205 control group and miR-205 mimic+ TSP-1 group ( t =8.118, 26.970, 39.550, 42.490, 14.570, 12.240, 36.830, 45.220, P <0.05 or P <0.01). At 24 h after transfection, compared with miR-205 control group, the cell apoptosis in miR-205 mimic group was increased, and the cell apoptosis in miR-205 inhibitor group was decreased. At 24 h after transfection, compared with miR-205 mimic group, the cell apoptosis in miR-205 control group and miR-205 mimic+ TSP-1 group were decreased. Conclusions: miR-205 can inhibit the proliferation and promote the apoptosis of Fbs in human hypertrophic scar by inhibiting the expression of TSP-1, which has the potential to be a therapeutic target for hypertrophic scar.

Objective: To investigate the expression and effect of microRNA-205 (miR-205) in hypertrophic scar. Methods: The experimental research method were applied. From October 2019 to January 2020, hypertrophic scar tissue from 6 patients with hypertrophic scar [1 male and 5 females, aged (36±7) years], and remaining normal skin tissue from 6 trauma patients [2 males and 4 females, aged (38±9) years] after flap transplantation operation were collected. The above-mentioned 12 patients were admitted to the General Hospital of Northern Theater Command and met the inclusion criteria. Real time fluorescent quantitative polymerase chain reaction was used to detect the mRNA expressions of miR-205 and thrombospondin-1 (TSP-1). The hypertrophic scar tissue was taken to culture the 3rd to 5th passage of fibroblasts (Fbs) for the follow-up experiments. Fbs of hypertrophic scar was divided into TSP-1+miR-205 control group, TSP-1+miR-205 mimic group, TSP-1 mutant+miR-205 control group, TSP-1 mutant +miR-205 mimic group, which were transfected with the corresponding sequences. At 48 h after transfection, the expressions of luciferase and renal luciferase were detected by luciferase reporter gene detection kit, and the luciferase/renal luciferase ratio was calculated to indicate the activity of TSP-1. Two batches of hypertrophic scar Fbs were collected and divided into miR-205 control group, miR-205 mimic group, and miR-205 inhibitor group and miR-205 control group, miR-205 mimic group, and miR-205 mimic+TSP-1 group, respectively, which were transfected with the corresponding sequences. At 0 (immediately), 12, 24, 36, and 48 h after transfection, the cell viability was detected by microplate reader. Two batches of hypertrophic scar Fbs were collected, grouped, and treated as the cell viability detecting experiment. At 24 h after transfection, Hoechst 33258 staining was performed to observe the nuclear shrinkage, so as to reflect the apoptosis of Fbs. The number of samples in cell experiment was 3. Data were statistically analyzed with analysis of variance for factorial design, one-way analysis of variance, and t test. Results: The mRNA expression of miR-205 in hypertrophic scar tissue was 0.54±0.05, which was significantly lower than 1.26±0.07 in normal skin tissue (t=8.213, P<0.01). The expression of TSP-1 mRNA in hypertrophic scar tissue was 1.46±0.07, which was significantly higher than 0.68±0.11 in normal skin tissue (t=6.031, P<0.01). At 48 h after transfection, the luciferase/renal luciferase ratio reflecting the TSP-1 activity of cells in TSP-1+miR-205 mimic group was 0.532±0.028, which was significantly lower than 0.998±0.012 in TSP-1+miR-205 control group (t=26.500, P<0.01), and the luciferase/renal luciferase ratio of cells in TSP-1 mutant+miR-205 mimic group was 0.963±0.012, which was close to 0.976±0.010 in TSP-1 mutant+miR-205 control group (t=0.816, P>0.05). At 12, 24, 36, and 48 h after transfection, the cell viability in miR-205 mimic group was significantly lower than that in miR-205 control group (t=6.169, 12.670, 27.130, 12.670, P<0.05 or P<0.01). At 0, 12, 24, 36, and 48 h after transfection, the cell viability in miR-205 inhibitor group was significantly higher than that in miR-205 control group (t=6.169, 7.221, 7.787, 7.835, 13.030, P<0.05 or P<0.01). At 12, 24, 36, and 48 h after transfection, the cell viability in miR-205 mimic group was significantly lower than that in miR-205 control group and miR-205 mimic+TSP-1 group (t=8.118, 26.970, 39.550, 42.490, 14.570, 12.240, 36.830, 45.220, P<0.05 or P<0.01). At 24 h after transfection, compared with miR-205 control group, the cell apoptosis in miR-205 mimic group was increased, and the cell apoptosis in miR-205 inhibitor group was decreased. At 24 h after transfection, compared with miR-205 mimic group, the cell apoptosis in miR-205 control group miR-205 mimic+TSP-1 group were decreased. Conclusions: miR-205 can inhibit the proliferation and promote the apoptosis of Fbs in hypertrophic scar by inhibiting the expression of TSP-1, which has the potential to be the therapeutic target for hypertrophic scar.

Thrombospondin-1 (TSP-1) is widely distributed in human tissues and is important in inhibiting angiogenesis.It also occupies an indispensable position in the formation, growth, differentiation, and metastasis of tumors in different tissues.TSP-1 plays an important role in the occurrence and development of various types of tumors. The inhibitory effect of TSP-1 on the angiogenesis and tumor development of oral and maxillofacial malignant tumors has been demonstrated in recent years. This paper reviews the findings and progress of TSP-1 research involving all kinds of tumors as well as oral and maxillofacial malignancies.

Objective: Taking human A549 cells as the research object, to construct the paraquat-induced pulmonary fibrosis model in vitro, and to explore the role of TSP-1 (Thrombospondin-1, TSP-1) and its receptor CD47 in PQ-induced pulmonary fibrosis. Methods: Human A549 cells were cultured in vitro, divided into normal control group, PQ group, Anti-TSP1 group (PQ with neutralizing anti-TSP1 antibody at a final concentration of 10 μg/ml) . A549 cells were stimulated with different concentrations (50, 100, 200, 400, 600, 800, 1 000 μmol/L) for different time (12, 24, 48 h) , and then CCK8 method was used to detect the cell viability to screen out the concentration and time of half cell viability. The subsequent test will be performed at this concentration point.The morphology of the cells was observed under inverted microscope. The expression levels of Fibronectin (FN) and type I collagen were determined by Enzyme Linked Immunosorbent Assay (ELISA) . Immunocytochemistry (ICC) and Immunofluorescence (IF) were used to observe the expression of TSP-1 and CD47 protein and the co-expression.The mRNA expression of TSP-1 and CD47 was detected by Real Time PCR (RT-PCR) . The protien expression of TSP-1 and CD47 was detected by Western Blot (WB) . The levels of Reactive Oxygen Species (ROS) were measured by flow cytometry. Results: Before neutralizing anti-TSP1 antibody intervention: (1) When the time of PQ was constant, the cell viability decreased with the increase of PQ concentration. (2) The cells in the control group were closely connected, cobble-like, arranged neatly; with the increase of PQ concentration, the cell gap of PQ group gradually increased, spindle shape or long spindle shape. (3) With the increase of PQ concentration, the relative expression of FN and I collagen in PQ group was gradually increased compared with the control group in a concentration-dependent manner, and 200 μmol/L is the most obvious. (4) Compared with the control group, the mRNA level and the protein expression of TSP-1 and CD47 in PQ group was significantly increased, and 200 μmol/L is the most obvious, and Immunofluorescence showed they were co-expression in cytoplasm. (5) Compared with the normal group, the level of ROS in A549 cells was significantly increased at 24 h after PQ stimulation. (6) Compared with PQ group, the cell viability of Anti-TSP1 group was significantly increased, and the morphology changed to normal cell morphology, and the mRNA level and the protein expression of TSP-1 and CD47 decreased, and the overexpression of ROS was inhibited, and the relative expression of FN and I collagen decreased. Conclusion: PQ stimulation induced morphological changes of A549 cells, increased expression of TSP-1, CD47, FN and type I collagen, and increased production of ROS.Neutralizing anti-TSP1 antibodies against TSP-1 can partially improve the above lesions. TSP-1-CD47 may be associated with oxidative stress-mediated PQ-induced pulmonary fibrosis.

Objective: To establish a rat model of paraquat (PQ) -induced pulmonary fibrosis and observe the changes in thrombospondin-1 (TSP-1) and its receptor CD47 in lung tissue, and to investigate their roles in the pathogenesis of PQ-induced pulmonary fibrosis. Methods: Fifty-four clean adult male Sprague-Dawley rats were randomly divided into normal control group ( n =6) and 2 h, 12 h, 1 d, 3 d, 7 d, and 14 d PQ poisoning groups ( n =8 per group). A rat model of PQ poisoning was established by a single gavage of 20 wt.% PQ solution (50 mg/kg). Flow cytometry was used to determine the concentration of reactive oxygen species (ROS) in blood and lung tissue. Enzyme-linked immunosorbent assay was used to determine the concentrations of hydroxyl radicals, malondialdehyde, and hydroxyproline in lung tissue. HE staining and Masson staining were used to observe the pathological damage of lung tissue after PQ poisoning. The expression of TSP-1 and CD47 in lung tissue was measured by Immunohistochemistry. Results: Compared with the normal control group, the 2 h to 7 d PQ poisoning groups showed significant increases in ROS fluorescence intensity in red blood cells and lung tissues and the concentrations of malondialdehyde and hydroxyl radicals in lung tissue ( P <0.05) , and the 14 d PQ poisoning group had a significant increase in the concentration of hydroxyproline in lung tissue ( P <0.05). HE staining showed that the 2 h to 7 d PQ poisoning groups had significantly higher semiquantitative pathological scores of pulmonary alveolitis than the normal control group ( P <0.05). The Masson staining showed that the 7 d and 14 d PQ poisoning groups had significantly higher semiquantitative pathological scores of pulmonary fibrosis than the normal control group ( P <0.05). Compared with the normal control group, all PQ poisoning groups (except the 12 h group) had significantly increased expression of TSP-1 in lung tissue ( P <0.05) , and all PQ poisoning groups (except the 1 d group) had significantly increased expression of CD47 in lung tissue ( P <0.05). Within 2 h after PQ poisoning, the expression of TSP-1 and CD47 was positively correlated with the concentrations of ROS, hydroxyl radicals, and malondialdehyde and the degree of pulmonary alveolitis ( P <0.01) ; at 1 d after PQ poisoning, the expression of TSP-1 and CD47 was positively correlated with the concentration of hydroxyproline in lung tissue ( P <0.01) . Conclusion: The expression of TSP-1 and CD47 is closely related to oxidative stress and subsequent pulmonary fibrosis, and they may be involved in the development and progression of pulmonary alveolitis and subsequent pulmonary fibrosis in rats with PQ poisoning.