线粒体
细胞凋亡
软骨细胞
细胞色素c
程序性细胞死亡
膜联蛋白
细胞生物学
胞浆
线粒体凋亡诱导通道
分子生物学
生物
化学
软骨
生物化学
解剖
酶
作者
Jun-Hui Liu,Xiong Guo,Watt Alanna J.,Y G Zhang,Peng Xu,Jianfeng Yao,Yuxin Bai
标识
DOI:10.1016/j.joca.2010.07.003
摘要
ObjectiveKashin–Beck disease (KBD) is an endemic degenerative osteoarthritis (OA) associated with extracellular matrix degradation and chondrocyte necrosis in the articular and growth plate cartilage. The role of mitochondria in degenerative diseases is widely recognized but its function in KBD is unknown. The aim of this investigation was to evaluate mitochondrial function to understand the mitochondria-mediated caspase activation and apoptosis in adult KBD chondrocytes.MethodsMitochondrial function was evaluated by analyzing the activities of respiratory chain enzyme complexes and citrate synthase (CS), intracellular adenosine triphosphate (ATP) contents, as well as changes in mitochondrial membrane potential (ΔΨm). Apoptotic cell death was evaluated by analyzing the cytochrome c release from mitochondria to the cytosol, caspase-9 and 3 activities, and the apoptosis rate of KBD articular chondrocytes.ResultsActivities of complexes II, III, IV and V were reduced in KBD articular chondrocytes compared with cells from normal controls. However, the mitochondrial mass was increased in KBD samples. Cultured KBD chondrocytes had a reduction of cellular ATP levels and contained a higher proportion of cells with de-energized mitochondria. Mitochondrial cytochrome c release and activation of caspase-9 and 3 were also observed. The percentages of positive apoptotic chondrocytes from the KBD patient group stained by Hoechst nuclear stain and Annexin V/PI for flow cytometry exhibited higher levels than that of the healthy controls.ConclusionThese findings suggest the involvement of mitochondrial function and apoptotic cell death in the pathophysiology of KBD. The dysfunction of the mitochondria may play an important role in KBD articular chondrocytes apoptosis.
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