MiR-193b regulates early chondrogenesis by inhibiting the TGF-beta2 signaling pathway
MiR-193b regulates early chondrogenesis by inhibiting the TGF-beta2 signaling pathway
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MiR-193b 通过抑制 TGF-β2 信号通路调节早期软骨形成
DOI：
10.1016/j.febslet.2015.02.017
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发表时间：
2015-04-13
期刊：
影响因子：
3.5
通讯作者：
Liao, Weiming
中科院分区：
文献类型：
--
作者：
Hou, Changhe;Yang, Zibo;Liao, Weiming
胡萝卜素的产生和降解受miRNA调控。我们先前的研究表明，在软骨形成的人脂肪间充质干细胞（hADSC）中，miR-193 b的表达发生了变化。在目前的研究中，我们研究了miR-193 b在软骨形成和软骨降解中的作用。荧光素酶报告基因测定显示miR-193 b靶向TGFB 2和TGFBR 3 3 '-UTR的种子序列。miR-193 b抑制软骨形成ATDC 5细胞中早期软骨形成标记物的表达，以及IL-1b诱导的PMC中TNF-α的表达。总之，miR-193 b可能通过靶向TGFB 2和TGFBR 3抑制早期软骨形成，并可能通过抑制炎症软骨细胞中TNF-α的表达来调节炎症。(C)2015由Elsevier B. V.代表欧洲生物化学学会联合会出版。
Cartilage generation and degradation are regulated by miRNAs. Our previous study has shown altered expression of miR-193b in chondrogenic human adipose-derived mesenchymal stem cells (hADSCs). In the current study, we investigated the role of miR-193b in chondrogenesis and cartilage degradation. Luciferase reporter assays showed that miR-193b targeted seed sequences of the TGFB2 and TGFBR3 3'-UTRs. MiR-193b suppressed the expression of early chondrogenic markers in chondrogenic ATDC5 cells, and TNF-alpha expression in IL-1b-induced PMCs. In conclusion, MiR-193b may inhibit early chondrogenesis by targeting TGFB2 and TGFBR3, and may regulate inflammation by repressing TNF-alpha expression in inflamed chondrocytes. (C) 2015 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.