Cooperation between VEGF and β3 integrin during cardiac vascular development
Year: 2006
Type: article
Abstract: In the developing myocardium, vascular endothelial growth factor (VEGF)-dependent neovascularization occurs by division of existing vessels, a process that persists for several weeks following birth. During this remodeling phase, mRNA expression of beta3 integrin in the heart decreases significantly as vessel maturation progresses. However, in male mice lacking beta3, coronary capillaries fail to mature and continue to exhibit irregular endothelial thickness, endothelial protrusions into the lumen, and expanded cytoplasmic vacuoles. Surprisingly, this phenotype was not seen in female beta3-null mice. Enhanced VEGF signaling contributes to the beta3-null phenotype, because these vessels can be normalized by inhibitors of VEGF or Flk-1. Moreover, intravenous injection of VEGF induces a similar angiogenic phenotype in hearts of adult wild-type mice. These findings show a clear vascular phenotype in the hearts of mice lacking beta3 and suggest this integrin plays a critical role in coronary vascular development and the vascular response to VEGF.
Source: Blood
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
Awards: G1091699278, G1648785187, G2003983467, Integrin alpha v beta 3 promotes resistance to EGF receptor inhibitors, CRAF-mediated vascular resistance to cancer therapies, Endothelial Barrier Function Regulation by VEGF, VEGF and PDGF in angiogenesis and tumor progression, G7063744252, G7663115156, Regulation of cell invasion by apoptotic mechanisms, Mechanisms of VEGF-induced vascular permeability, Integrin Signaling in Hemostasis and Blood Diseases
OpenAlex ID: W2081258528