Abstract
During retinal development, a physiologic hypoxia stimulates endothelial cell proliferation. The hypoxic milieu warrants retina vascularization and promotes the activation of several mechanisms aimed to ensure homeostasis and energy balance of both endothelial and retinal cells. Autophagy is an evolutionarily conserved catabolic system that contributes to cellular adaptation to a variety of environmental changes and stresses. In association with the physiologic hypoxia, autophagy plays a crucial role during development. Autophagy expression profile was evaluated in the developing retina from birth to post-natal day 18 of rat pups, using qPCR, western blotting and immunostaining methodologies. The rat post-partum developing retina displayed increased active autophagy during the first postnatal days, correlating to the hypoxic phase. In latter stages of development, rat retinal autophagy decreases, reaching a normalization between post-natal days 14-18, when the retina is fully vascularized and mature. Collectively, the present study elaborates on the link between hypoxia and autophagy, and contributes to further elucidate the role of autophagy during retinal development.
Highlights
Fluorescein-labeled isolectin B4 was used to assess the progress of retinal vascularization in the rat
Rat retinal vascularization is almost completed around P13-P16 [36]
Quantitative analysis demonstrated a significant difference at P7, where the retina was 90% vascularized (p < 0.001) and in the late stages of ocular blood vessel development, P14-P18 (p < 0.001), where the retinas were fully vascularized (100%) as compared to birth
Summary
The heightened metabolic demand of the retina is supplied by a structured vascular systems, including retinal vessels and the choriocapillaris, which provide nutrients and oxygen to the inner and the outer layers of the retina respectively [3,4]. In the early stages of embryogenesis, the interior of the eye is metabolically supplied by a transient embryonic circulatory network in the vitreous, referred to as the hyaloid system [6]. In the latter stages of development, the hyaloid vasculature regresses and concurrently is replaced by the retinal vasculature [7]. The physiologic hypoxia in uterus (O2 levels < 5%) drives the proliferation of retinal blood vessels from the optic nerve to the periphery [8], through vascular endothelial growth factor (VEGF)-mediated angiogenesis [9,10]
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