Histone deacetylase 9 plays a role in the antifibrogenic effect of astaxanthin in hepatic stellate cells.
作者： Yue Yang , Minkyung Bae , Young-Ki Park , Yoojin Lee , Tho X. Pham
DOI: 10.1016/J.JNUTBIO.2016.11.003
关键词: Mef2 、 Transforming growth factor 、 HDAC9 、 Gene expression 、 Transcriptional regulation 、 Molecular biology 、 Histone deacetylase 、 Hepatic stellate cell 、 Biology 、 Gene knockdown
摘要: Activation of hepatic stellate cells (HSCs) is critical for liver fibrosis development. Previously, we showed that astaxanthin (ASTX), a xanthophyll carotenoid, has antifibrogenic effects in LX-2 cells, human HSC cell line. We sought to determine the effect ASTX on activation, and identify molecular mediators are critically involved processes. prevented activation mouse primary HSCs, as evidenced by attenuated induction procollagen type I α1. In also inhibited transforming growth factor β1 (TGFβ1)-induced fibrogenic gene expression. Among 11 classical histone deacetylases (HDACs), difference HDAC9 mRNA levels between quiescent activated HSCs was most evident while significantly decreased expression its transcriptional regulator myocyte enhancer 2 (MEF2). protein well. reduced MEF2. Human biliary cirrhosis livers higher than normal livers, other pathologies exhibited induced knockdown TGFβ1-induced conclusion, inhibits facilitates inactivation, which attributable inhibitory action
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