Coregulation of fibronectin signaling and matrix contraction by tenascin-C and syndecan-4

被引:110
作者
Midwood, KS [1 ]
Valenick, LV [1 ]
Hsia, HC [1 ]
Schwarzbauer, JE [1 ]
机构
[1] Princeton Univ, Dept Biol Mol, Princeton, NJ 08544 USA
关键词
D O I
10.1091/mbc.E04-08-0759
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Syndecan-4 is a ubiquitously expressed heparan sulfate proteoglycan that modulates cell interactions with the extracellular matrix. It is transiently up-regulated during tissue repair by cells that mediate wound healing. Here, we report that syndecan-4 is essential for optimal fibroblast response to the three-dimensional fibrin-fibronectin provisional matrix that is deposited upon tissue injury. Interference with syndecan-4 function inhibits matrix contraction by preventing cell spreading, actin stress fiber formation, and activation of focal adhesion kinase and RhoA mediated-intracellular signaling pathways. Tenascin-C is an extracellular matrix protein that regulates cell response to fibronectin within the provisional matrix. Syndecan-4 is also required for tenascin-C action. Inhibition of syndecan-4 function suppresses tenascin-C activity and overexpression of syndecan-4 circumvents the effects of tenascin-C. In this way, tenascin-C and syndecan-4 work together to control fibroblast morphology and signaling and regulate events such as matrix contraction that are essential for efficient tissue repair.
引用
收藏
页码:5670 / 5677
页数:8
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