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Dev Cell April 19, 2011; 20 (4): 526-39.

Blood vessel tubulogenesis requires Rasip1 regulation of GTPase signaling.

Xu K , Sacharidou A , Fu S , Chong DC , Skaug B , Chen ZJ , Davis GE , Cleaver O .

Cardiovascular function depends on patent blood vessel formation by endothelial cells (ECs). However, the mechanisms underlying vascular "tubulogenesis" are only beginning to be unraveled. We show that endothelial tubulogenesis requires the Ras interacting protein 1, Rasip1, and its binding partner, the RhoGAP Arhgap29. Mice lacking Rasip1 fail to form patent lumens in all blood vessels, including the early endocardial tube. Rasipl null angioblasts fail to properly localize the polarity determinant Par3 and display defective cell polarity, resulting in mislocalized junctional complexes and loss of adhesion to extracellular matrix (ECM). Similarly, depletion of either Rasip1 or Arhgap29 in cultured ECs blocks in vitro lumen formation, fundamentally alters the cytoskeleton, and reduces integrin-dependent adhesion to ECM. These defects result from increased RhoA/ROCK/myosin II activity and blockade of Cdc42 and Rac1 signaling. This study identifies Rasip1 as a unique, endothelial-specific regulator of Rho GTPase signaling, which is essential for blood vessel morphogenesis.

PubMed ID: 21396893
PMC ID: PMC3078994
Article link: Dev Cell
Grant support: [+]
Genes referenced: arhgap1 arhgap29 cdc42 ephb4 gja5 kdr mgc69466 pard3 rac1 rasip1 rho rho.2 rhoa sacs

Article Images: [+] show captions
References [+] :
Aird, Phenotypic heterogeneity of the endothelium: II. Representative vascular beds. 2007, Pubmed

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