Abstract:
:Retinopathy of prematurity is a blinding disease, initiated by lack of retinal vascular growth after premature birth. We show that lack of insulin-like growth factor I (IGF-I) in knockout mice prevents normal retinal vascular growth, despite the presence of vascular endothelial growth factor, important to vessel development. In vitro, low levels of IGF-I prevent vascular endothelial growth factor-induced activation of protein kinase B (Akt), a kinase critical for endothelial cell survival. Our results from studies in premature infants suggest that if the IGF-I level is sufficient after birth, normal vessel development occurs and retinopathy of prematurity does not develop. When IGF-I is persistently low, vessels cease to grow, maturing avascular retina becomes hypoxic and vascular endothelial growth factor accumulates in the vitreous. As IGF-I increases to a critical level, retinal neovascularization is triggered. These data indicate that serum IGF-I levels in premature infants can predict which infants will develop retinopathy of prematurity and further suggests that early restoration of IGF-I in premature infants to normal levels could prevent this disease.
journal_name
Proc Natl Acad Sci U S Aauthors
Hellstrom A,Perruzzi C,Ju M,Engstrom E,Hard AL,Liu JL,Albertsson-Wikland K,Carlsson B,Niklasson A,Sjodell L,LeRoith D,Senger DR,Smith LEdoi
10.1073/pnas.101113998keywords:
subject
Has Abstractpub_date
2001-05-08 00:00:00pages
5804-8issue
10eissn
0027-8424issn
1091-6490pii
101113998journal_volume
98pub_type
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