Overexpression of miR‐483‐5p/3p cooperate to inhibit mouse liver fibrosis by suppressing the TGF‐β stimulated HSCs in transgenic mice |
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| Authors: | Fuyuan Li Ning Ma Ruiqi Zhao Guodong Wu Yanfen Zhang Yu Qiao Dong Han Ya Xu Ying Xiang Bingzhu Yan Jianfeng Jin Guixiang Lv Lei Wang Changqing Xu Xu Gao Shanshun Luo |
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| Institution: | 1. Department of Biochemistry and Molecular Biology, Harbin Medical University, , Harbin, China;2. Translational Medicine Center of Northern China, , Harbin, China;3. Department of Laboratory Diagnosis, Affiliated Hospital of Harbin Medical University, , Harbin, China;4. Department of Cell Biology, Medical School, Yangtze University, , Jingzhou, China;5. Department of Infectious Diseases, Second Affiliated Hospital of Harbin Medical University, , Harbin, China;6. Department of Pathophysiology, Harbin Medical University, , Harbin, China;7. Basic Medical Institute of Heilongjiang Medical Science Academy, , Harbin, China;8. Key Laboratory of Cardiovascular Medicine Research (Harbin Medical University), Ministry of Education, , Harbin, China;9. Department of Gerontology, First Affiliated Hospital of Harbin Medical University, , Harbin, China |
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| Abstract: | The transition from liver fibrosis to hepatocellular carcinoma (HCC) has been suggested to be a continuous and developmental pathological process. MicroRNAs (miRNAs) are recently discovered molecules that regulate the expression of genes involved in liver disease. Many reports demonstrate that miR‐483‐5p and miR‐483‐3p, which originate from miR‐483, are up‐regulated in HCC, and their oncogenic targets have been identified. However, recent studies have suggested that miR‐483‐5p/3p is partially down‐regulated in HCC samples and is down‐regulated in rat liver fibrosis. Therefore, the aberrant expression and function of miR‐483 in liver fibrosis remains elusive. In this study, we demonstrate that overexpression of miR‐483 in vivo inhibits mouse liver fibrosis induced by CCl4. We demonstrate that miR‐483‐5p/3p acts together to target two pro‐fibrosis factors, platelet‐derived growth factor‐β and tissue inhibitor of metalloproteinase 2, which suppress the activation of hepatic stellate cells (HSC) LX‐2. Our work identifies the pathway that regulates liver fibrosis by inhibiting the activation of HSCs. |
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| Keywords: | liver fibrosis microRNA HSCs transgenic mice |
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