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433 results on '"Cao, Xiaojian"'

57. Activation of glucagon-like peptide-1 receptor in microglia attenuates neuroinflammation-induced glial scarring via rescuing Arf and Rho GAP adapter protein 3 expressions after nerve injury

Author

Qian, Zhanyang, primary, Chen, Hongtao, additional, Xia, Mingjie, additional, Chang, Jie, additional, Li, Xinyu, additional, Ye, Suhui, additional, Wu, Shunjie, additional, Jiang, Shuai, additional, Bao, Junping, additional, Wang, Binyu, additional, Kong, Renyi, additional, Zhang, Sheng, additional, Zheng, Shengnai, additional, Cao, Xiaojian, additional, and Hong, Xin, additional

Published
2022
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58. Genome-wide association identifies OBFC1 as a locus involved in human leukocyte telomere biology

Author

Levy, Daniel, Neuhausen, Susan L., Hunt, Steven C., Kimura, Masayuki, Hwang, Shih-Jen, Chen, Wei, Bis, Joshua C., Fitzpatrick, Annette L., Smith, Erin, Johnson, Andrew D., Gardner, Jeffrey P., Srinivasan, Sathanur R., Schork, Nicholas, Rotter, Jerome I., Herbig, Utz, Psaty, Bruce M., Sastrasinh, Malinee, Murray, Sarah S., Vasan, Ramachandran S., Province, Michael A., Glazer, Nicole L., Lu, Xiaobin, Cao, Xiaojian, Kronmal, Richard, Mangino, Massimo, Soranzo, Nicole, Spector, Tim D., Berenson, Gerald S., Aviv, Abraham, and Kooperberg, Charles

Published
2010

59. Reprogramming Mycobacterium tuberculosis CRISPR System for Gene Editing and Genome-wide RNA Interference Screening

Author

Rahman, Khaista, primary, Jamal, Muhammad, additional, Chen, Xi, additional, Zhou, Wei, additional, Yang, Bin, additional, Zou, Yanyan, additional, Xu, Weize, additional, Lei, Yingying, additional, Wu, Chengchao, additional, Cao, Xiaojian, additional, Tyagi, Rohit, additional, Ahsan Naeem, Muhammad, additional, Lin, Da, additional, Habib, Zeshan, additional, Peng, Nan, additional, Fu, Zhen F., additional, and Cao, Gang, additional

Published
2021
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69. miR-1297 Suppresses Osteosarcoma Proliferation and Aerobic Glycolysis by Regulating PFKFB2

Author

Pan,Xiaohui, Li,Haibo, Tan,Jingxue, Weng,Xiaokun, Zhou,Li, Weng,Yiping, and Cao,Xiaojian

Subjects
OncoTargets and Therapy
Abstract

Xiaohui Pan,1,* Haibo Li,1,* Jingxue Tan,1,* Xiaokun Weng,2 Li Zhou,1 Yiping Weng,1 Xiaojian Cao3 1Department of Orthopedics, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People’s Hospital, Changzhou, Jiangsu 213003, People’s Republic of China; 2Department of Radiotherapy, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People’s Hospital, Changzhou, Jiangsu 213003, People’s Republic of China; 3Department of Orthopedics, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yiping Weng; Xiaojian Cao Email wyp2020cz@163.com; dr_cxj001@163.comBackground: MiR-1297 is reported to function as a tumor suppressor of various cancers. However, the role of miR-1297 in the development of osteosarcoma (OS) has not been elaborated. The purpose of this study was to investigate the functional effects of miR-1297 on OS progression and the underlying mechanism.Methods: The expression of protein and mRNA in OS cells was evaluated by Western blotting and quantitative real-time polymerase chain reaction. Cellular proliferation was investigated by cell counting kit-8, colony formation and apoptosis assays. Bioinformatics methods were used to predict target genes. The relationship between PFKFB2 and miR-1297 was demonstrated by dual-luciferase reporter assay. Metabolic changes in OS cells were monitored using an XF96 metabolic flux analyzer.Results: We found that miR-1297 was downregulated in OS and that lower expression of miR-1297 promoted proliferation and contributed to the Warburg effect in OS cells. Furthermore, we showed that silencing PFKFB2 inhibited proliferation and reduced aerobic glycolysis while overexpression of PFKFB2 reduced the anti-tumor function of miR-1297 in OS cells. Mechanistically, miR-1297 acted as a tumor suppressor in OS and reduced the expression of PFKFB2 by directly targeting its 3ʹUTR.Conclusion: The miR-1297/PFKFB2 axis regulated OS proliferation by controlling the Warburg effect. Our results revealed a previously undiscovered function of miR-1297 in OS, which strongly linked metabolic alterations with cancer progression. Targeting miR-1297 may become a promising therapeutic approach for OS.Keywords: osteosarcoma, miR-1297, PFKFB2, Warburg effect

Published
2020

73. Reprogramming Mycobacterium TuberculosisCRISPR System for Gene Editing and Genome-Wide RNA Interference Screening

Author

Rahman, Khaista, Jamal, Muhammad, Chen, Xi, Zhou, Wei, Yang, Bin, Zou, Yanyan, Xu, Weize, Lei, Yingying, Wu, Chengchao, Cao, Xiaojian, Tyagi, Rohit, Naeem, Muhammad Ahsan, Lin, Da, Habib, Zeshan, Peng, Nan, Fu, Zhen F., and Cao, Gang

Abstract

Mycobacterium tuberculosisis the causative agent of tuberculosis (TB), which is still the leading cause of mortality from a single infectious disease worldwide. The development of novel anti-TB drugs and vaccines is severely hampered by the complicated and time-consuming genetic manipulation techniques for M. tuberculosis.Here, we harnessed an endogenous type III-A CRISPR/Cas10 system of M. tuberculosisfor efficient gene editingand RNA interference (RNAi). This simple and easy method only needs to transform a single mini-CRISPR array plasmid, thus avoiding the introduction of exogenous protein and minimizing proteotoxicity. We demonstrated that M. tuberculosisgenes can be efficiently and specifically knocked in/out by this system as confirmed by DNA high-throughput sequencing. This system was further applied to single- and multiple-gene RNAi. Moreover, we successfully performed genome-wide RNAi screeningto identify M. tuberculosisgenes regulating in vitroand intracellular growth. This system can be extensively used for exploring the functional genomics of M. tuberculosisand facilitate the development of novel anti-TB drugs and vaccines.

Published
2022
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74. JEV Infection Induces M-MDSC Differentiation Into CD3+ Macrophages in the Brain.

Author

Zhang, Nan, Gao, Xiaochen, Zhang, Weijia, Xiong, Junyao, Cao, Xiaojian, Fu, Zhen F., and Cui, Min

Subjects
MYELOID-derived suppressor cells, JAPANESE encephalitis viruses, MACROPHAGES, JAPANESE B encephalitis, BONE marrow
Abstract

Japanese encephalitis virus (JEV) is one of the most important members of the flavivirus family. It is a typical zoonotic pathogen that has caused substantial social and economic losses worldwide. The relation between JEV-induced immunosuppression and inflammatory responses has not been thoroughly investigated. In this study, cells infiltrating the brain tissue of JEV-infected mice were mainly identified as monocytic myeloid-derived suppressor cells (M-MDSCs), which subsequently differentiated into CD3+ macrophages. Co-culture with T cells showed that both splenic M-MDSCs and brain infiltrated M-MDSCs isolated from JEV-infected mice inhibited T cell proliferation through ARG1 and iNOS. The splenectomy model revealed that JEV-induced M-MDSCs were mainly derived from bone marrow and migrated to the spleen and central nervous system (CNS). The results of the transcriptome analysis and IRF7-deficient mice indicated that the ZBP1-IRF7 signaling pathway stimulated by JEV RNA played a central role in the induction of M-MDSCs. M-MDSCs migrated into the CNS through the chemokine CCL2/N-CCL2 derived from astrocytes and brain infiltrated M-MDSCs differentiated into CD3+ macrophages through a mechanism mediated by M-CSF, IL-6 and IFN-γ in the brain microenvironment. These findings provide evidence for the mechanism that JEV regulates the differentiation of M-MDSCs and thereby exacerbates pathogenicity, which represents a potential therapeutic target for Japanese encephalitis (JE). [ABSTRACT FROM AUTHOR]

Published
2022
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80. Telomere dynamics in macaques and humans

Author

Gardner, Jeffrey P., Kimura, Masayuki, Chai, Weihang, Durrani, Jameel F., Tchakmakjian, Levon, Cao, Xiaojian, Lu, Xiaobin, Li, Guanghui, Peppas, Athanasios P., Skurnick, Joan, Wright, Woodring E., Shay, Jerry W., and Aviv, Abraham

Subjects
Macaques -- Genetic aspects, Macaques -- Comparative analysis, Human beings -- Genetic aspects, Human beings -- Comparative analysis, Man -- Genetic aspects, Man -- Comparative analysis, Telomeres -- Demographic aspects, Aging -- Influence, Aging -- Genetic aspects, Health, Seniors
Abstract

In humans, telomere length in proliferating tissues shortens with age--a process accelerated with age-related diseases. Thus, telomere length and attrition with age in the nonhuman primate may serve as a useful paradigm for understanding telomere biology in humans. We examined telomere parameters in tissues of young and old Macaca fascicularis and compared them with several tissues from humans. Macaque telomeres were variable in length and exhibited partial synchrony (equivalence) within animals. They were longer than humans, partially because of longer subtelomeric segments. As skeletal muscle telomere length was unchanged with age, we used it as an internal reference to offset interanimal variation in telomere length. We identified age-dependent telomere attrition in lung, pancreas, skin, and thyroid. Similar to humans, telomerase activity was detected in spleen, thymus, digestive tract, and gonads. We conclude that factors that modify telomere attrition and aging in humans may also operate in the macaque.

Published
2007

82. Calcium adaptation to sodium pump inhibition in a human megakaryocytic cell line

Author

Kimura, Masayuki, Cao, Xiaojian, and Aviv, Abraham

Subjects
Blood clot -- Research, Thrombosis -- Research, Blood platelets -- Research, Bone marrow cells -- Research, Biological sciences
Abstract

The unique characteristics of the platelet Na/Ca exchanger, i.e., its dependence on both transmembrane Na and K gradients, render it highly sensitive to Na pump inhibition. In this project, we observed that the human megakaryocytic cell line CHRF-288 expresses both the [[alpha].sub.1]- and [[alpha].sub.3]-isoforms of the Na-K-ATPase. Inhibition of the Na pump increased the RNA and protein expressions of sarco(endo)plasmic reticulum Ca-ATPase 2b, cytosolic Na and Ca, and the freely exchangeable Ca in the endoplasmic reticulum. These changes occurred in concert with diminished store-operated Ca entry and an increase in the maximal activity of the Na/Ca exchanger. Inhibition of the Na pump by ouabain was more effective in inducing these changes than diminishing medium K. Collectively, these observations point to an integrative effort to counteract the impact of Na pump inhibition by Ca sequestration into the endoplasmic reticulum, diminished Ca entry, and increased activity of the Na/Ca exchanger. The implications of these findings in platelet biology are discussed. platelets; thrombosis; potassium; stroke

Published
2005

94. Reprogramming the endogenous type III-A CRISPR-Cas system for genome editing, RNA interference and CRISPRi screening in Mycobacterium tuberculosis

Author

Rahman, Khaista, primary, Jamal, Muhammad, additional, Chen, Xi, additional, Zhou, Wei, additional, Yang, Bin, additional, Zou, Yanyan, additional, Xu, Weize, additional, Lei, Yingying, additional, Wu, Chengchao, additional, Cao, Xiaojian, additional, Tyagi, Rohit, additional, Naeem, Muhammad Ahsan, additional, Lin, Da, additional, Habib, Zeshan, additional, Peng, Nan, additional, Fu, Zhen F., additional, and Cao, Gang, additional

Published
2020
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98. Pirfenidone inhibits epidural scar fibroblast proliferation and differentiation by regulating TGF-β1-induced Smad-dependent and -independent pathways

Author

Shi, Kun, Wang, Fengzhen, Xia, Jihua, Zuo, Bangjie, Wang, Zhaohong, and Cao, Xiaojian

Subjects
Original Article
Abstract

Epidural fibrosis causes serious complications in patients who have undergone laminectomy. Pirfenidone is an effective antifibrotic agent but its effect on epidural fibrosis remains unclear. In this study, we aimed to investigate the effect of pirfenidone on epidural fibrosis and to evaluate its mechanism of action on human epidural scar fibroblasts. In a rat model of laminectomy, the degree of epidural fibrosis was quantified via Rydell standard classification, histological analysis, and collagen density analyses. In cultured human epidural scar fibroblasts, cell proliferation was measured using a Cell Counting Kit-8 and EdU assay. Cell apoptosis was detected using Annexin V/propidium iodide staining, and cytotoxicity was evaluated via lactate dehydrogenase assay. Relative mRNA levels of α-smooth muscle actin (α-SMA) and collagen type I were analyzed using quantitative polymerase chain reaction. The protein expression of α-SMA and collagen type I and the phosphorylation status of Smad2, Smad3, protein kinase B (Akt), and p38 were determined via western blotting. Pirfenidone reduced epidural fibrosis by inhibiting fibroblast proliferation and suppressing collagen formation in rats. It also inhibited human epidural scar fibroblast proliferation with no cytotoxic or apoptotic effects. Pirfenidone inhibited fibroblast differentiation by decreasing TGF-β1-induced transcriptional and translational expression of α-SMA. It inhibited TGF-β1-induced phosphorylation of Smad2, Smad3, Akt, and p38. This study suggests that topical application of pirfenidone could reduce epidural scar adhesion after laminectomy, and that its mechanism of action may be the inhibition of TGF-β1-induced epidural scar fibroblast proliferation and differentiation into myofibroblasts through the attenuation of TGF-β1-induced Smad-dependent and -independent pathways.

Published
2019

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