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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Endothelial Growth Factors / genetics
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Endothelial Growth Factors / metabolism
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Growth Hormone / agonists
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Growth Hormone / antagonists & inhibitors
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Growth Hormone / blood
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Growth Hormone / pharmacology
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Growth Hormone / physiology*
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Hormone Antagonists / pharmacology
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Insulin-Like Growth Factor I / metabolism
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Insulin-Like Growth Factor I / pharmacology
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Ischemia
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Lymphokines / genetics
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Lymphokines / metabolism
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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Peptides, Cyclic / pharmacology
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Recombinant Proteins / pharmacology
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Retinal Neovascularization / etiology*
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Retinal Neovascularization / metabolism
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Retinal Neovascularization / pathology
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Retinal Vessels
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
Substances
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Endothelial Growth Factors
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Hormone Antagonists
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Lymphokines
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Peptides, Cyclic
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Recombinant Proteins
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
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seglitide
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Insulin-Like Growth Factor I
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Growth Hormone