Since suppression of IGF-i can suppress neovascularization, in phase II of ROP we hypothesized that IGF-I is critical to normal retinal vascular development and that a lack of IGF-I in the early neonatal period is associated with poor vascular growth and with subsequent proliferative ROP. After birth, IGF-I levels decrease from in utero levels due to the loss of IGF-I provided by the placenta and the amniot-ic fluid.
We examined normal retinal vascular development in IGF-I knockout mice and found that IGF-I is critical in the normal development of the retinal vessels. . Retinal blood vessels grow more slowly in IGF-i knockout mice than in normal mice, a pattern very similar to that seen in premature babies with ROP. It was determined that a minimum level of IGF-I is required for maximum VEGF activation of the Akt endothelial cell survival pathway. This finding explains how loss of IGF-I could cause the disease by preventing the normal survival of vascular endothelial cells.
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