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Research paper thumbnail of Essential Role of Growth Hormone in Ischemia-Induced Retinal Neovascularization

Science, 1997

Retinal neovascularization is the major cause of untreatable blindness. The role of growth hormon... more 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-l (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. membrane (arrows). (B) Cross section Of an eye from a GH antagonist GI 19K transgenic mouse. No R. G. Smith and J. M. Schaeffer, Merck Research Labo-vascular cell nuclei are apparent internal to the inner limiting membrane. (C) Nontransgenicflat-mounted ratories, Rahway, NJ 07065, USA.

Research paper thumbnail of Essential Role of Growth Hormone in Ischemia-Induced Retinal Neovascularization

Science, 1997

Retinal neovascularization is the major cause of untreatable blindness. The role of growth hormon... more 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-l (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. membrane (arrows). (B) Cross section Of an eye from a GH antagonist GI 19K transgenic mouse. No R. G. Smith and J. M. Schaeffer, Merck Research Labo-vascular cell nuclei are apparent internal to the inner limiting membrane. (C) Nontransgenicflat-mounted ratories, Rahway, NJ 07065, USA.

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