Abstract
Purpose: :
To determine the impact of bim deficiency on postnatal retinal vascularization, as well as retinal neovascularization during oxygen-induced ischemic retinopathy (OIR) and laser-induced choroidal neovascularization.
Methods: :
We examined retinal vascularization during normal development, OIR and choroidal neovascularization using wholemount immunostaining. Apoptosis was monitored by TUNEL analysis.
Results: :
Loss of bim expression was associated with increased retinal vascular density in mature animals. This was mainly attributed to increased numbers of pericytes and endothelial cells. However, the initial spread of the superficial layer of retinal vasculature and, the appearance and density of the tip cells were similar in bim +/+ and bim -/- mice. In addition, hyaloid vessel regression was attenuated in the absence of bim. Furthermore, in the absence of bim retinal vessel obliteration and neovascularization did not occur during OIR. Instead, normal inner retinal vascularization proceeded independent of changes in oxygen levels. In contrast, choroidal neovascularization occurred equally well in bim +/+ and bim -/- mice.
Conclusions: :
Together our data suggest bim expression is responsible for the inherent sensitivity of the developing retinal vasculature to changes in oxygen levels, and promotes vessel obliteration in response to hyperoxia.
Keywords: retinal neovascularization • apoptosis/cell death • choroid: neovascularization