1. Leptin reduces microRNA-122 level in hepatic stellate cells in vitro and in vivo.
- Author
-
Zhai, Xuguang, Cheng, Fangyun, Ji, Li, Zhu, Xiaofei, Cao, Qing, Zhang, Yali, Jia, Xin, Zhou, Qian, Guan, Wei, and Zhou, Yajun
- Subjects
- *
OVERWEIGHT persons , *LEPTIN , *MICRORNA , *LIVER cells , *FIBROSIS , *STEROL regulatory element-binding proteins , *PHYSIOLOGY , *DISEASES - Abstract
Obese patients, often accompanied by hyperleptinemia, are more likely to develop liver fibrosis. Leptin, an adipocyte-derived hormone, augments inflammatory in liver and promotes hepatic stellate cell (HSC) activation (a key step for liver fibrogenesis) and liver fibrosis. microRNA-122 (miR-122) is the most abundant liver-specific miRNA and can attenuate liver fibrosis. This study examined the effect of leptin on miR-122 level in HSCs in vivo and in vitro . Results demonstrated that leptin reduced the levels of both miR-122 (mature miR-122) and primary miR-122 (pri-miR-122). The effects of leptin on the levels of miR-122 and pri-miR-122 were through at least hedgehog pathway. Leptin-induced decrease in sterol regulatory element-binding protein-1c (SREBP-1c) has been shown to contribute to leptin-induced HSC activation. We revealed a mutual promotional effect between SREBP-1c and miR-122. Further experiments indicated that miR-122 inhibited leptin-induced liver fibrosis in leptin-deficient mouse model. These data have potential implications for clarifying the mechanisms of hepatic fibrogenesis associated with elevated leptin level in human such as obese patients [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF