We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
α-parvin controls vascular mural cell recruitment to vessel wall by regulating RhoA/ROCK signalling.
- Authors
Montanez, Eloi; Wickström, Sara A.; Altstätter, Johannes; Haiyan Chu; Fässler, Reinhard
- Abstract
During blood vessel development, vascular smooth muscle cells (vSMCs) and pericytes (PCs) are recruited to nascent vessels to stabilize them and to guide further vessel remodelling. Here, we show that loss of the focal adhesion (FA) protein α-parvin (α-pv) in mice leads to embryonic lethality due to severe cardiovascular defects. The vascular abnormalities are characterized by poor vessel remodelling, impaired coverage of endothelial tubes with vSMC/PCs and defective association of the recruited vSMC/PCs with endothelial cells (ECs). α-pv-deficient vSMCs are round and hypercontractile leading either to their accumulation in the tissue or to local vessel constrictions. Because of the high contractility, α-pv-deficient vSMCs fail to polarize their cytoskeleton resulting in loss of persistent and directed migration. Mechanistically, the absence of α-pv leads to increased RhoA and Rho-kinase (ROCK)-mediated signalling, activation of myosin II and actomyosin hypercontraction in vSMCs. Our findings show that α-pv represents an essential adhesion checkpoint that controls RhoA/ROCK-mediated contractility in vSMCs.
- Subjects
BLOOD vessels; LABORATORY mice; VASCULAR smooth muscle; ENDOTHELIUM; CYTOSKELETON
- Publication
EMBO Journal, 2009, Vol 28, Issue 20, p3132
- ISSN
0261-4189
- Publication type
Article
- DOI
10.1038/emboj.2009.295