Effect of microRNA-145 on IL-1β-induced cartilage degradation in human chondrocytes
Effect of microRNA-145 on IL-1β-induced cartilage degradation in human chondrocytes
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DOI：
10.1016/j.febslet.2014.05.033
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发表时间：
2014-06-27
期刊：
影响因子：
3.5
通讯作者：
Dong, Shiwu
中科院分区：
文献类型：
--
作者：
Yang, Bo;Kang, Xia;Dong, Shiwu
MicroRNA-145已被证明可以调节软骨细胞的动态平衡。似乎miR-145与骨关节炎(OA)的软骨功能障碍有关。然而，miR-145在白细胞介素1β(IL-1β)诱导的骨性关节炎软骨细胞外基质(ECM)降解中的作用一直不清楚。在这里，我们发现在骨关节炎软骨细胞中miR-145的表达增加，并对IL-1β刺激做出反应。我们证实，母亲抗十碳瘫痪同系物3(SMAD3)，一个维持软骨细胞内稳的关键因素，直接受miR-145调节。MiR-145的调控影响Smad3的表达，导致其下游靶基因表达的改变以及IL-1β诱导的骨关节炎软骨细胞的ECM降解。这表明miR-145可能部分通过靶向Smad3参与了OA软骨中受损的ECM。(C)2014年欧洲生化学会联合会。爱思唯尔出版，版权所有。
MicroRNA-145 has been shown to regulate chondrocyte homeostasis. It seems that miR-145 is implicated in cartilage dysfunction in Osteoarthritis (OA). However, the functional role of miR-145 in interleukin-1 beta (IL-1 beta)-induced extracellular matrix (ECM) degradation of OA cartilage has never been clarified. Here, we show that miR-145 expression increased in OA chondrocytes and in response to IL-1 beta stimulation. We confirm that mothers against decapentaplegic homolog 3 (Smad3), a key factor in maintaining chondrocyte homeostasis, is directly regulated by miR-145. Modulation of miR-145 affects the expression of Smad3 causing a change of its downstream target gene expression as well as IL-1 beta-induced ECM degradation in OA chondrocytes. This indicates that miR-145 contributes to impaired ECM in OA cartilage probably in part via targeting Smad3. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.