Integrin beta1 subunit controls mural cell adhesion, spreading, and blood vessel wall stability

Circulation Research
Sabu AbrahamRalf H Adams

Abstract

Growth, maturation, and integrity of the blood vessel network require extensive communication between the endothelial cells, which line the vascular lumen, and associated mural cells, namely vascular smooth muscle cells and pericytes. Pericytes extend long processes, make direct contact with the capillary endothelium, and promote vascular quiescence by suppressing angiogenic sprouting. Vascular smooth muscle cells are highly contractile, extracellular matrix-secreting cells that cover arteries and veins and provide them with mechanical stability and elasticity. In the damaged blood vessel wall, for example in atherosclerotic lesions, vascular smooth muscle cells lose their differentiated state and acquire a highly mitotic, so-called "synthetic" phenotype, which is thought to promote pathogenesis. Among other factors, extracellular matrix molecules and integrin family cell-matrix receptors may regulate this phenotypic transition. Here we show that the inactivation of the gene encoding the integrin beta1 subunit (Itgb1) with a Cre-loxP approach in mice leads to mural cell defects and postnatal lethality. Integrin beta1-deficient vascular smooth muscle cells display several hallmarks of the synthetic phenotype: Cell proliferation ...Continue Reading

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