Beta-catenin, cartilage, and osteoarthritis.
Beta-catenin, cartilage, and osteoarthritis.
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DOI：
10.1111/j.1749-6632.2009.05212.x
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发表时间：
2010-03
影响因子：
5.2
通讯作者：
Chen D
中科院分区：
文献类型：
--
作者：
Wu Q;Zhu M;Rosier RN;Zuscik MJ;O'Keefe RJ;Chen D
骨关节炎（OA）发生过程中的早期细胞事件是关节软骨细胞成熟加速和细胞外基质降解，通常出现在关节软骨的负重区域。我们最近对转基因OA小鼠模型的研究结果表明，关节软骨细胞中β-catenin信号转导的上调最有可能是正常关节软骨细胞转化为成熟（关节炎）软骨细胞的原因，这与软骨细胞成熟基因的激活和基质降解有关。关节软骨细胞中β-连环蛋白基因的条件激活导致OA样表型。Smurf 2（一种E3泛素连接酶）的过表达也通过上调β-连环蛋白信号传导诱导OA样表型。此外，在OA患者的关节软骨组织中也发现β-连环蛋白上调。这些发现表明β-连环蛋白在关节软骨功能中起着重要作用，β-连环蛋白信号的激活可能代表了OA发展的病理机制。
The early cellular events during the development of osteoarthritis (OA) are accelerated articular chondrocyte maturation and extracellular matrix degradation, which are usually seen in the weight-bearing region of articular cartilage. The results of our recent studies from transgenic OA mouse models indicate that upregulation of β-catenin signaling in articular chondrocytes is most likely responsible for the conversion of normal articular chondrocytes into maturing (arthritic) chondrocytes, which is associated with activation of chondrocyte maturational genes and matrix degradation. Conditional activation of the β-catenin gene in articular chondrocytes leads to an OA-like phenotype. Overexpression of Smurf2, an E3 ubiquitin ligase, also induces an OA-like phenotype through upregulation of β-catenin signaling. In addition, β-catenin upregulation was also found in articular cartilage tissues in patients with OA. These findings indicate that β-catenin plays a central role in articular cartilage function and that activation of β-catenin signaling may represent a pathologic mechanism for OA development.
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影响因子：
7.8
作者：
Kwan, KM;Pang, MKM;Zhou, S;Cowan, SK;Kong, RYC;Pfordte, T;Olsen, BR;Sillence, DO;Tam, PPL;Cheah, KSE
通讯作者：
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影响因子：
14.9
作者：
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通讯作者：
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影响因子：
7
作者：
Bakker, AC;van de Loo, FAJ;van den Berg, WB
通讯作者：
van den Berg, WB