Rac1 functions as a reversible tension modulator to stabilize VE-cadherin trans-interaction (vol 208, pg 23, 2015)

被引：15

作者：

Daneshjou, Nazila ^{[1
]}

Sieracki, Nathan ^{[1
]}

Amerongen, Geerten P. van Nieuw ^{[1
]}

Conway, Daniel E. ^{[1
]}

Schwartz, Martin A. ^{[1
]}

Komarova, Yulia A. ^{[1
]}

Malik, Asrar B. ^{[1
]}

机构：

[1] Virginia Commonwealth Univ, Dept Biomed Engn, Richmond, VA USA

来源：

JOURNAL OF CELL BIOLOGY | 2015年 / 209卷 / 01期

关键词：

D O I：

10.1083/jcb.20140910803202015c

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The role of the RhoGTPase Rac1 in stabilizing mature endothelial adherens junctions (AJs) is not well understood. In this paper, using a photoactivatable probe to control Rac1 activity at AJs, we addressed the relationship between Rac1 and the dynamics of vascular endothelial cadherin (VE-cadherin). We demonstrated that Rac1 activation reduced the rate of VE-cadherin dissociation, leading to increased density of VE-cadherin at AJs. This response was coupled to a reduction in actomyosin-dependent tension across VE-cadherin adhesion sites. We observed that inhibiting myosin II directly or through photo-release of the caged Rho kinase inhibitor also reduced the rate of VE-cadherin dissociation. Thus, Rac1 functions by stabilizing VE-cadherin trans-dimers in mature AJs by counteracting the actomyosin tension. The results suggest a new model of VE-cadherin adhesive interaction mediated by Rac1-induced reduction of mechanical tension at AJs, resulting in the stabilization of VE-cadherin adhesions.

引用

页码：181 / 181

页数：1