首页> 外文期刊>FEBS letters. >Down-regulation of miR-23b may contribute to activation of the TGF-beta1/Smad3 signalling pathway during the termination stage of liver regeneration.
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Down-regulation of miR-23b may contribute to activation of the TGF-beta1/Smad3 signalling pathway during the termination stage of liver regeneration.

机译:在肝再生的终止阶段,miR-23b的下调可能有助于TGF-beta1 / Smad3信号通路的激活。

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摘要

MicroRNAs (miRNAs) are known to play important roles in liver regeneration, although the role of miRNAs associated with the termination of liver regeneration is not as well studied. Here we reported the down-regulation of miR-23b in the termination stage of liver regeneration in rats. In addition, Smad3 was identified as a target of miR-23b during liver regeneration. Up-regulation of miR-23b promoted BRL-3A cell proliferation and partially inhibited transforming growth factor (TGF)-beta1-induced apoptosis. Furthermore, TGF-beta1 transcriptionally inhibited miR-23b expression. We conclude that down-regulation of miR-23b may contribute to activation of the TGF-beta1/Smad3 signalling pathway during the termination stage of liver regeneration.
机译:尽管尚未充分研究与肝再生终止相关的miRNA的作用,但MicroRNA(miRNA)在肝再生中起着重要作用。在这里,我们报道了大鼠肝脏再生终止阶段miR-23b的下调。另外,在肝脏再生期间,Smad3被鉴定为miR-23b的靶标。 miR-23b的上调促进BRL-3A细胞增殖,并部分抑制转化生长因子(TGF)-beta1诱导的细胞凋亡。此外,TGF-beta1转录抑制miR-23b表达。我们得出结论,在肝再生终止阶段,miR-23b的下调可能有助于TGF-beta1 / Smad3信号通路的激活。

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