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首页> 外文期刊>Osteoarthritis and cartilage >Nitric oxide alters chondrocyte function by disrupting cytoskeletal signaling complexes.
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Nitric oxide alters chondrocyte function by disrupting cytoskeletal signaling complexes.

机译:一氧化氮通过破坏细胞骨架信号复合物来改变软骨细胞功能。

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摘要

Components of osteoarthritis include increases in pericellular fibronectin and in chondrocyte beta1 integrin expression. Events which follow ligation of fibronectin to its chondrocyte-receptor, the integrin alpha5beta1 include an assembly of a subplasmalemmal actin/rho A/focal adhesion kinase signaling complex. In addition, nitric oxide (NO), a potential mediator of cartilage pathophysiology disrupts the cytoskeletal signaling complex associated with integrin signaling. In these studies, we examined the relationship among integrin signaling, biosynthesis of S-35 sulfate containing proteoglycans and release of YKL-40 (a secretory glycoprotein) by comparing cell responses using cells plated on a fibronectin-coated or polyHEME coated surfaces. We report that the release of proteoglycan and glycoprotein require anchorage dependent signals by integrin costimulation. NO which disrupts the integrin signaling complex attenuates both cell responses. Taken together NO may serve as a nonspecific 'brake' to prevent anabolic and catabolic injury responses. Copyright 1999 OsteoArthritis Research Society International.
机译:骨关节炎的组成部分包括细胞周围纤连蛋白和软骨细胞beta1整合素表达的增加。纤连蛋白与其软骨细胞受体整联蛋白α5β1连接后的事件包括浆膜下肌动蛋白/ rho A /局灶性粘附激酶信号复合物的装配。另外,一氧化氮(NO)是软骨病理生理的潜在介质,它破坏了整合素信号传导相关的细胞骨架信号传导复合物。在这些研究中,我们通过使用铺在纤连蛋白涂层或polyHEME涂层表面上的细胞比较细胞应答,检查了整联蛋白信号传导,含蛋白多糖的S-35硫酸盐的生物合成和YKL-40(一种分泌型糖蛋白)的释放之间的关系。我们报告说,蛋白聚糖和糖蛋白的释放需要整合素共刺激的锚定依赖信号。破坏整合素信号复合物的NO减弱了两种细胞的反应。合在一起,NO可以充当非特异性“刹车”,以防止合成代谢和分解代谢损伤反应。版权所有1999国际骨关节炎研究协会。

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