Open AccessOverexpression of miR‐483‐5p/3p cooperate to inhibit mouse liver fibrosis by suppressing the TGF ‐β stimulated HSC s in transgenic mice
Author(s) -
Li Fuyuan,
Ma Ning,
Zhao Ruiqi,
Wu Guodong,
Zhang Yanfen,
Qiao Yu,
Han Dong,
Xu Ya,
Xiang Ying,
Yan Bingzhu,
Jin Jianfeng,
Lv Guixiang,
Wang Lei,
Xu Changqing,
Gao Xu,
Luo Shanshun
Publication year - 2014
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12293
Subject(s) - hepatic stellate cell , microrna , fibrosis , cancer research , biology , genetically modified mouse , hepatocellular carcinoma , transforming growth factor , transgene , in vivo , hepatic fibrosis , microbiology and biotechnology , gene , pathology , medicine , endocrinology , genetics
Abstract The transition from liver fibrosis to hepatocellular carcinoma ( HCC ) has been suggested to be a continuous and developmental pathological process. Micro RNA s (mi RNA s) 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 CC l 4 . 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 HSC s.