Table 1.

Role of integrins in angiogenesis and lymphangiogenesis. This table summarizes the effect of genetic ablation of different integrin subunits on the vascular and lymphatic development in mouse embryo and during postnatal life.

Integrin	Major ligands	Mouse Phenotype
α1β1	Collagen, laminin	α1−/− : normal vascular development; reduced adult angiogenesis
α2β1	Collagen, laminin	α2−/− : normal vascular development; enhanced tumor angiogenesis
α4β1	CS1 fibronectin, VCAM-1	α4−/−: embryonic lethal; 50% die at E9.5–10.5, failure of chorion-allantois fusion; 50% die at E11.5 owing to cardiovascular defects
α5β1	Fibronectin, L1-CAM	α5−/− : embryonic lethal E10–11; yolk sac and embryonic vessel defects
α6β1	Laminin	α6−/− : embryonic lethal; lethal skin defects; no vascular defect
α9β1	Tensacin, fibronectin, thrombospondin, VCAM-1, collagen, laminin	α9−/− : post-natal lethality P8–P12; chylothrorax (accumulation of lymph in the pleural cavity)
αMβ2	ICAM-1, fibrinogen	αM−/− : normal development
αvβ3	Fibronectin, vitronectin, von Willebrand factor, tensacin, DEL-1, osteopontin	αv−/− : 80% embryonic lethality E9.5; 20% die P20 with brain hemorrhage β3−/− : 50% embryonic and early post-natal lethality; enhanced angiogenesis in surviving adults
αvβ5	Vitronectin, osteopontin, DEL-1	αv−/− : 80% embryonic lethality E9.5; 20% die P20 with brain hemorrhage β5−/− : normal development; reduced adult angiogenesis in response to certain angiogenic factors.
αvβ8	Collagen, laminin, fibronectin	β8−/− : disrupted brain blood vessel formation
α6β4	Laminin 5	β4−/−: normal vascular development but lethal skin defects