Integrin activation and matrix binding mediate cellular responses to mechanical stretch

被引:184
作者
Katsumi, A
Naoe, T
Matsushita, T
Kaibuchi, K
Schwartz, MA [1 ]
机构
[1] Univ Virginia, Cardiovasc Res Ctr, Charlottesville, VA 22908 USA
[2] Univ Virginia, Mellon Prostate Res Inst, Dept Microbiol, Charlottesville, VA 22908 USA
[3] Univ Virginia, Mellon Prostate Res Inst, Dept Biomed Engn, Charlottesville, VA 22908 USA
[4] Nagoya Univ, Grad Sch Med, Dept Cell Pharmacol, Showa Ku, Aichi 4668550, Japan
[5] Nagoya Univ, Grad Sch Med, Dept Hematol, Showa Ku, Aichi 4668550, Japan
关键词
D O I
10.1074/jbc.C400455200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Mechanical tension is a critical determinant of cell growth, differentiation, apoptosis, migration, and development. Integrins have been implicated in sensing force but little is known about how forces are transduced to biochemical signals. We now show that mechanical strain stimulates conformational activation of integrin alpha v beta 3 in NIH3T3 cells. Integrin activation is mediated by phosphoinositol 3-kinase and is followed by an increase in integrin binding to extracellular matrix proteins. Mechanical stretch stimulation of JNK was dependent on new integrin binding to extracellular matrix. These data define a molecular mechanism for the role of integrins in mechanotransduction.
引用
收藏
页码:16546 / 16549
页数:4
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