Syndecan-1 controls cell migration by activating Rap1 to regulate focal adhesion disassembly

被引:25
作者
Altemeier, William A. [1 ]
Schlesinger, Saundra Y. [1 ]
Buell, Catherine A. [1 ]
Parks, William C. [1 ]
Chen, Peter [1 ]
机构
[1] Univ Washington, Ctr Lung Biol, Div Pulm & Crit Care Med, Seattle, WA 98195 USA
基金
美国国家卫生研究院;
关键词
Syndecan-1; Focal adhesion; Migration; SMALL G-PROTEINS; NASCENT ADHESIONS; INTEGRIN ACTIVITY; ALPHA-ACTININ; DYNAMICS; FAK; PHOSPHORYLATION; ALPHA(V)BETA(3); PAXILLIN; TURNOVER;
D O I
10.1242/jcs.109884
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
After injury, residual epithelial cells coordinate contextual clues from cell-cell and cell-matrix interactions to polarize and migrate over the wound bed. Protrusion formation, cell body translocation and rear retraction is a repetitive process that allows the cell to move across the substratum. Fundamental to this process is the assembly and disassembly of focal adhesions that facilitate cell adhesion and protrusion formation. Here, we identified syndecan-1 as a regulator of focal adhesion disassembly in migrating lung epithelial cells. Syndecan-1 altered the dynamic exchange of adhesion complex proteins, which in turn regulates migration speed. Moreover, we provide evidence that syndecan-1 controls this entire process through Rap1. Thus, syndecan-1 restrains migration in lung epithelium by activating Rap1 to slow focal adhesion disassembly.
引用
收藏
页码:5188 / 5195
页数:8
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