seglitide and Ischemia

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.

Topics: Animals; Endothelial Growth Factors; Growth Hormone; Hormone Antagonists; Insulin-Like Growth Factor I; Ischemia; Lymphokines; Mice; Mice, Inbred C57BL; Mice, Transgenic; Peptides, Cyclic; Recombinant Proteins; Retinal Neovascularization; Retinal Vessels; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factors