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Laminin and Matrix metalloproteinase 11 regulate Fibronectin levels in the zebrafish myotendinous junction

机译:层粘连蛋白和基质金属蛋白酶11调节斑马鱼肌末端连接中的纤连蛋白水平

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摘要

BackgroundRemodeling of the extracellular matrix (ECM) regulates cell adhesion as well as signaling between cells and their microenvironment. Despite the importance of tightly regulated ECM remodeling for normal muscle development and function, mechanisms underlying ECM remodeling in vivo remain elusive. One excellent paradigm in which to study ECM remodeling in vivo is morphogenesis of the myotendinous junction (MTJ) during zebrafish skeletal muscle development. During MTJ development, there are dramatic shifts in the primary components comprising the MTJ matrix. One such shift involves the replacement of Fibronectin (Fn)-rich matrix, which is essential for both somite and early muscle development, with laminin-rich matrix essential for normal function of the myotome. Here, we investigate the mechanism underlying this transition.
机译:背景细胞外基质(ECM)的重塑可调节细胞黏附力以及细胞与其微环境之间的信号传导。尽管严格调节ECM重塑对于正常的肌肉发育和功能很重要,但体内ECM重塑的机制仍然难以捉摸。在体内研究ECM重塑的一种出色范例是斑马鱼骨骼肌发育过程中肌末端连接(MTJ)的形态发生。在MTJ开发过程中,构成MTJ矩阵的主要组件发生了巨大变化。一种这样的转变涉及用富含纤连蛋白(Fn)的基质替代肌纤维蛋白正常功能所必需的富含纤连蛋白(Fn)的基质,该基质对体节和早期肌肉发育都是必不可少的。在这里,我们研究了这种转变的基础机制。

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