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Author Lu, Le ♦ Wang, Jinlong ♦ Lu, Hongwei ♦ Zhang, Guoyu ♦ Liu, Yang ♦ Wang, Jiazhong ♦ Zhang, Yafei ♦ Shang, Hao ♦ Ji, Hong ♦ Chen, Xi ♦ Duan, Yanxia ♦ Li, Yiming
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ BILIARY TRACT ♦ CARBON TETRACHLORIDE ♦ CELL CULTURES ♦ CELL PROLIFERATION ♦ FIBROSIS ♦ GENES ♦ GROWTH FACTORS ♦ INJECTION ♦ LIVER ♦ MESSENGER-RNA ♦ RATS ♦ RECEPTORS
Abstract Hepatic stellate cells (HSCs) are the primary sources of extracellular matrix (ECM) in normal and fibrotic liver. Peroxisome proliferator-activated receptor gamma (PPARγ) maintains HSCs in a quiescent state, and its downregulation induces HSC activation. MicroRNAs (miRNAs) can induce PPARγ mRNA degradation, but the mechanism by which miRNAs regulate PPARγ in rat HSCs is unclear. This study aimed to investigate some miRNAs which putatively bind to the 3′-untranslated region (3′-UTR) of PPARγ mRNA, and increase expression of ECM genes in rat HSCs. In carbon tetrachloride injection (CCl{sub 4}) and common bile duct ligation (CBDL) liver fibrosis models, miRNAs miR-130a, miR-130b, miR-301a, miR-27b and miR-340 levels were found to be increased and PPARγ expression decreased. Overexpression of miR-130a and miR-130b enhanced cell proliferation by involving Runx3. MiR-130a and miR-130b decreased PPARγ expression by targeting the 3′-UTR of PPARγ mRNA in rat HSC-T6 cells. Transforming growth factor-β1 (TGF-β1) may mediate miR-130a and miR-130b overexpression, PPARγ downregulation, and ECM genes overexpression in cell culture. These findings suggest that miR-130a and miR-130b are involved in downregulation of PPARγ in liver fibrosis. - Highlights: • MiR-130a and miR-130b are increased and PPARγ is decreased in liver fibrosis models. • MiR-130a and miR-130b decreased PPARγ by targeting the 3′-UTR of PPARγ mRNA. • MiR-130a and miR-130b enhanced HSC cell proliferation by involving Runx3. • TGF-β1 may mediate miR-130a and miR-130b overexpression.
ISSN 0006291X
Educational Use Research
Learning Resource Type Article
Publisher Date 2015-09-25
Publisher Place United States
Journal Biochemical and Biophysical Research Communications
Volume Number 465
Issue Number 3


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