• participation of mir-200a in tgf-β1-mediated hepatic stellate cell activation

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    جزئیات بیشتر مقاله
    • تاریخ ارائه: 1392/07/24
    • تاریخ انتشار در تی پی بین: 1392/07/24
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     hepatic stellate cell (hsc) activation is a pivotal event in the initiation and progression of hepatic fibrosis since it mediates transforming growth factor beta 1 (tgf-β1)-driven extracellular matrix (ecm) deposition. micrornas (mirnas), small non-coding rnas modulating messenger rna (mrna) and protein expression, have emerged as key factors to regulate cell proliferation, differentiation, and apoptosis. although the function of mir-200a has been discussed in many cancers and fibrotic diseases, its role in hepatic fibrosis is still poorly understood. the aim of this study is to investigate whether mir-200a could attenuate hepatic fibrosis partly through wnt/β-catenin and tgf-β-dependant mechanisms. our study found that the expression of endogenous mir-200a was decreased in vitro in tgf-β1-induced hsc activation as well as in vivo in ccl4-induced rat liver fibrosis. overexpression of mir-200a significantly inhibited α-sma activity and further affected the proliferation of tgf-β1-dependent activation of hsc. in addition, we identified β-catenin and tgf-β2 as two functional downstream targets for mir-200a. interestingly, mir-200a specifically suppressed β-catenin in the protein level, whereas mir-200a-mediated suppression of tgf-β2 was shown on both mrna and protein levels. our results revealed the critical regulatory role of mir-200a in hsc activation and implied mir-200a as a potential candidate for therapy by deregulation of wnt/β-catenin and tgfβ signaling pathways, at least in part, via decreasing the expression of β-catenin and tgf-β2.

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