Different gene knockout/transgenic mouse models manifesting persistent fetal vasculature: Are integrins to blame for this pathological condition?

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Abstract

Persistent fetal vasculature (PFV) occurs as a result of a failure of fetal vasculature to undergo normal programmed involution. During development, before the formation of retinal vessels, the lens and the inner retina are nourished by the hyaloid vasculature. Hyaloid vessels extend from the optic nerve and run through the vitreous to encapsulate the lens. As fetal retinal vessels develop, hyaloid vasculature naturally regresses. Failure of regression of the hyaloid artery has been shown to lead to severe congenital pathologies. Studies on childhood blindness and visual impairment in the United States have shown that PFV accounts for 4.8% of total blindness. Although PFV is a serious developmental disease affecting the normal visual development pathway, the exact regulatory mechanism responsible for the regression of the hyaloid artery is still unknown. In this review, we have summarized the cellular defects associated with different knockout models that manifest features of persistent fetal vasculature. Based on similar cellular defects observed in different knockouts (KO)s such as altered migration, increased proliferation and decreased apoptosis and, the known role of integrins in the regulation of these cellular behaviors, we propose here that integrins may play a significant role in the pathophysiology of persistent fetal vasculature disease.

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