Down‐Regulation of Rac GTPase‐Activating Protein OCRL1 Causes Aberrant Activation of Rac1 in Osteoarthritis Development
Down‐Regulation of Rac GTPase‐Activating Protein OCRL1 Causes Aberrant Activation of Rac1 in Osteoarthritis Development
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DOI：
10.1002/art.39174
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发表时间：
2015-05
影响因子：
13.3
通讯作者：
Shouan Zhu;J. Dai;Huan-huan Liu;Xiaoxia Cong;Yishan Chen;Yan Wu;Hu Hu-Hu;B. Heng;H. Ouyang;Yiting Zhou
中科院分区：
文献类型：
--
作者：
Shouan Zhu;J. Dai;Huan-huan Liu;Xiaoxia Cong;Yishan Chen;Yan Wu;Hu Hu-Hu;B. Heng;H. Ouyang;Yiting Zhou
软骨细胞肥大和矿化被认为是骨关节炎（OA）的重要病理因素。我们以前报道，Rac1被异常激活，促进软骨细胞肥大，矿化，基质金属蛋白酶13和ADAMTS的表达在OA。然而，OA中Rac1异常激活的潜在机制尚不清楚。本研究旨在确定控制Rac1在OA中活性的特定分子调节剂，并研究其在软骨细胞肥大、矿化和OA发展中的功能。
Chondrocyte hypertrophy and mineralization are considered to be important pathologic factors in osteoarthritis (OA). We previously reported that Rac1 was aberrantly activated to promote chondrocyte hypertrophy, mineralization, and expression of matrix metalloproteinase 13 and ADAMTS in OA. However, the underlying mechanism of aberrant Rac1 activation in OA is unclear. The present study was undertaken to identify the specific molecular regulator controlling Rac1 activity in OA, as well as to investigate its function in chondrocyte hypertrophy, mineralization, and OA development.