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首页> 外文期刊>Journal of Cellular Physiology >Effect of mechanical strain on the collagen VI pericellular matrix in anterior cruciate ligament fibroblasts
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Effect of mechanical strain on the collagen VI pericellular matrix in anterior cruciate ligament fibroblasts

机译：胶原蛋白VI机械应变的影响在前交叉韧带pericellular矩阵成纤维细胞

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摘要

Cell-extracellular matrix interaction plays a major role in maintaining the structural integrity of connective tissues and sensing changes in the biomechanical environment of cells. Collagen VI is a widely expressed non-fibrillar collagen, which regulates tissues homeostasis. The objective of the present investigation was to extend our understanding of the role of collagen VI in human ACL. This study shows that collagen VI is associated both in vivo and in vitro to the cell membrane of knee ACL fibroblasts, contributing to the constitution of a microfibrillar pericellular matrix. In cultured cells the localization of collagen VI at the cell surface correlated with the expression of NG2 proteoglycan, a major collagen VI receptor. The treatment of ACL fibroblasts with anti-NG2 antibody abolished the localization of collagen VI indicating that collagen VI pericellular matrix organization in ACL fibroblasts is mainly mediated by NG2 proteoglycan. In vitro mechanical strain injury dramatically reduced the NG2 proteoglycan protein level, impaired the association of collagen VI to the cell surface, and promoted cell cycle withdrawal. Our data suggest that the injury-induced alteration of specific cell-ECM interactions may lead to a defective fibroblast self-renewal and contribute to the poor regenerative ability of ACL fibroblasts. J. Cell. Physiol. 229: 878-886, 2014.
机译：Cell-extracellular矩阵相互作用中起着维护结构的主要作用结缔组织和遥感的完整性的生物力学环境的变化细胞。non-fibrillar胶原蛋白,调节组织体内平衡。调查是扩展我们理解胶原蛋白的作用VI在人类ACL。表明胶原VI体内都有关联和体外膝关节ACL的细胞膜成纤维细胞,导致了宪法一个microfibrillar pericellular矩阵。细胞的定位在细胞胶原蛋白VI表面与喜欢的《忍者外传2》的表达第六主要胶原蛋白受体蛋白多糖。与anti-NG2治疗前交叉韧带成纤维细胞抗体废除了本地化的胶原蛋白VI表明胶原VI pericellular在前交叉韧带成纤维细胞主要是矩阵组织由NG2成为蛋白多糖。劳损大大减少了喜欢的《忍者外传2》蛋白多糖蛋白质水平,受损协会第六胶原细胞表面,,促进了细胞周期撤军。表明,创伤性的变化可能导致特定cell-ECM交互有缺陷的纤维母细胞自我更新和贡献ACL的可怜的再生能力成纤维细胞。2014.

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