What has target gene deletion in mice revealed about the role of V integrins in angiogenesis?
Studies in mice with targeted gene deletions of either V, ß3, or ß5 were initially less informative than anticipated with regard to the role of these integrins in angiogenesis. Embryos deficient in V develop normally until E9.5 and have unimpaired vasculogenesis and angiogenesis in many organs. Approximately 80% of the embryos die, apparently as the result of placental defects. The mice that survive suffer lethal intracranial and intestinal hemorrhage (Bader et al., 1998). Mice lacking either integrin ß3 (Hodivala-Dilke et al., 1999) or ß5 (Huang et al., 2000) undergo normal angiogenesis, and the pattern of retinal neovascularization in ß3-null mice is indistinguishable from that in wild-type mice. In a follow-up to the original characterization of the ß3-/- mice, Hodivala-Dilke’s group reported that tumors grown in ß3-/- mice or in mice with a combined deficiency of ß3 and ß5 are larger in size and display enhanced angiogenesis (Reynolds et al., 2002). They observed an augmented angio
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