Publication: Abrogation of ALK5 in hepatic stellate cells decreases hepatic fibrosis and ameliorates liver damage in mice following treatment with thioacetamide
Issued Date
2018-03-01
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ISSN
01253395
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2-s2.0-85048337768
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Mahidol University
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SCOPUS
Bibliographic Citation
Songklanakarin Journal of Science and Technology. Vol.40, No.2 (2018), 314-320
Suggested Citation
Somyoth Sridurongrit, Chen Ke, Wanthita Kongphat, Arnon Pudgerd, Chanyatip Suwannasing Abrogation of ALK5 in hepatic stellate cells decreases hepatic fibrosis and ameliorates liver damage in mice following treatment with thioacetamide. Songklanakarin Journal of Science and Technology. Vol.40, No.2 (2018), 314-320. doi:10.14456/sjst-psu.2018.31 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/47528
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Title
Abrogation of ALK5 in hepatic stellate cells decreases hepatic fibrosis and ameliorates liver damage in mice following treatment with thioacetamide
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Abstract
© 2018, Prince of Songkla University. All rights reserved. While transforming growth factor-β (TGF-β) is known to be a key inducer of hepatic stellate cell (HSC) activation during liver fibrosis but it is unclear which TGF-β receptor is required for this HSC-mediated fibrogenesis. Here, we report that abrogation of TGF-β type I receptor ALK5 in HSC activation led to reduced collagen deposition and a decreased number of myofibroblasts in livers of mutant mice lacking ALK5 in HSC (Alk5/GFAP-Cre mice) following thioacetamide (TAA) exposure. The reduced fibrosis was accompanied by decreased expression of HSC activation markers in livers. In addition, Alk5/GFAP-Cre mice exhibited decreased immune cell infiltration and reduced production of inflammatory cytokines. Associated with reduced fibrosis and inflammation, amelioration of liver injury was observed in Alk5/GFAP-Cre mice after TAA treatment. In conclusion, our results indicated that TGF-β signaling via ALK5 in HSC enhanced liver fibrogenesis and inflammation led to amplification of hepatic injury in mice exposed to TAA.