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miR-23b 的下调可能有助于在肝再生终止阶段激活 TGF-β1/Smad3 信号通路。

Down-regulation of miR-23b may contribute to activation of the TGF-β1/Smad3 signalling pathway during the termination stage of liver regeneration.

机构信息

Department of Biochemistry and Molecular Biology, Second Military Medical University, 800 Xiangyin Road, Shanghai 200433, People's Republic of China.

出版信息

FEBS Lett. 2011 Mar 23;585(6):927-34. doi: 10.1016/j.febslet.2011.02.031. Epub 2011 Feb 25.

DOI:10.1016/j.febslet.2011.02.031
PMID:21354414
Abstract

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)-β1-induced apoptosis. Furthermore, TGF-β1 transcriptionally inhibited miR-23b expression. We conclude that down-regulation of miR-23b may contribute to activation of the TGF-β1/Smad3 signalling pathway during the termination stage of liver regeneration.

摘要

微小 RNA(miRNAs)在肝脏再生中起着重要作用,尽管与肝脏再生终止相关的 miRNAs 的作用尚未得到充分研究。在这里,我们报道了 miR-23b 在大鼠肝脏再生终止阶段的下调。此外,Smad3 被鉴定为 miR-23b 在肝脏再生过程中的靶标。miR-23b 的上调促进了 BRL-3A 细胞的增殖,并部分抑制了转化生长因子(TGF)-β1 诱导的细胞凋亡。此外,TGF-β1 转录抑制 miR-23b 的表达。我们的结论是,miR-23b 的下调可能有助于在肝脏再生终止阶段激活 TGF-β1/Smad3 信号通路。

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