February 1996
Volume 37, Issue 2
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Articles  |   February 1996
Roles of vascular endothelial growth factor and astrocyte degeneration in the genesis of retinopathy of prematurity.
Author Affiliations
  • J Stone
    Department of Molecular Biology, Hebrew University, Jerusalem.
  • T Chan-Ling
    Department of Molecular Biology, Hebrew University, Jerusalem.
  • J Pe'er
    Department of Molecular Biology, Hebrew University, Jerusalem.
  • A Itin
    Department of Molecular Biology, Hebrew University, Jerusalem.
  • H Gnessin
    Department of Molecular Biology, Hebrew University, Jerusalem.
  • E Keshet
    Department of Molecular Biology, Hebrew University, Jerusalem.
Investigative Ophthalmology & Visual Science February 1996, Vol.37, 290-299. doi:
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      J Stone, T Chan-Ling, J Pe'er, A Itin, H Gnessin, E Keshet; Roles of vascular endothelial growth factor and astrocyte degeneration in the genesis of retinopathy of prematurity.. Invest. Ophthalmol. Vis. Sci. 1996;37(2):290-299.

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      © 2016 Association for Research in Vision and Ophthalmology.

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Abstract

PURPOSE: To assess the role of vascular endothelial growth factor (VEGF) in the feline model of retinopathy of prematurity (ROP). METHODS: Retinopathy of prematurity was induced in neonatal cats by raising them in an oxygen-enriched (70% to 80%) atmosphere for 4 days to suppress vessel formation and then returning them to room air for 3 to 27 days. In situ hybridization was used to detect the expression of VEGF and its high-affinity receptor, flk-1, in the retina of neonatal cats, and glial fibrillary acidic protein immunocytochemistry was used to assess astrocyte status. RESULTS: The expression of VEGF in the innermost layers of retina fell in hyperoxia and increased on return to room air. Vascular endothelial growth factor expression was transient; it was maximal where vessels were about to form, and it rapidly downregulated after vessels had formed. During the proliferative vasculopathy of ROP, VEGF expression was stronger than in the normally developing retina, and the astrocytes that normally express VEGF degenerated. After the degeneration of astrocytes, VEGF was expressed by neurones of the ganglion cell layer. flk-1 was expressed by intraretinal and preretinal vessels. Supplemental oxygen therapy reduced or eliminated the overexpression of VEGF expression, astrocyte degeneration, and formation of preretinal vessels. CONCLUSIONS: Regulation of VEGF by tissue oxygen mediates the inhibition of vessel growth during hyperoxia and the subsequent proliferative vasculopathy. Degeneration of retinal astrocytes creates conditions for the growth of preretinal vessels.

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