Abstract
Apoptosis plays a critical role during development and in the maintenance of multicellular organisms. B cell leukemia lymphoma 2 (bcl‐2) protects endothelial cells (EC) from apoptosis in response to a variety of stimuli. Previous work from this laboratory demonstrated attenuation of postnatal retinal vascular development and retinal neovascularization during oxygen‐induced ischemic retinopathy in bcl‐2 deficient (bcl‐2 −/−) mice. How bcl‐2 affects EC function during these processes require further investigation. To gain further insight into the functions of bcl‐2 in the endothelium we isolated retinal EC from bcl‐2 +/+ and bcl‐2 −/− mice. Retinal EC lacking bcl‐2 demonstrated reduced cell migration, reduced tenascin‐C expression, and reduced adhesion to vitronectin and fibronectin. The bcl‐2 −/− retinal EC also failed to undergo capillary morphogenesis in Matrigel. In addition, using an ex vivo angiogenesis assay we observed reduced sprouting from aortic rings grown in culture from bcl‐2 −/− mice compared to bcl‐2 +/+ mice. Furthermore, re‐expression of bcl‐2 was sufficient to restore migration and capillary morphogenesis defects observed in bcl‐2−/− retinal EC. Thus, bcl‐2‐mediated functions play an important role in EC migration and capillary morphogenesis during retinal vascular development and angiogenesis.
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