Essential Role of Growth Hormone in Ischemia-Induced Retinal Neovascularization

Author:

Smith Lois E. H.123,Kopchick John J.123,Chen Wen123,Knapp Joanne123,Kinose Fumi123,Daley Douglas123,Foley Eliot123,Smith Roy G.123,Schaeffer James M.123

Affiliation:

1. L. E. H. Smith, F. Kinose, D. Daley, E. Foley, Department of Ophthalmology, Harvard Medical School and Children's Hospital, Boston, MA 02115, USA.

2. J. J. Kopchick, W. Chen, J. Knapp, Edison Biotechnology Institute, Ohio University, Athens, OH 45701, USA.

3. R. G. Smith and J. M. Schaeffer, Merck Research Laboratories, Rahway, NJ 07065, USA.

Abstract

Retinal neovascularization is the major cause of untreatable blindness. The role of growth hormone (GH) in ischemia-associated retinal neovascularization was studied in transgenic mice expressing a GH antagonist gene and in normal mice given an inhibitor of GH secretion (MK678). Retinal neovascularization was inhibited in these mice in inverse proportion to serum levels of GH and a downstream effector, insulin-like growth factor–I (IGF-I). Inhibition was reversed with exogenous IGF-I administration. GH inhibition did not diminish hypoxia-stimulated retinal vascular endothelial growth factor (VEGF) or VEGF receptor expression. These data suggest that systemic inhibition of GH or IGF-I, or both, may have therapeutic potential in preventing some forms of retinopathy.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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