Over expression of vascular endothelial growth factor and its receptor during the development of estrogen-induced rat pituitary tumors may mediate estrogen-initiated tumor angiogenesis.

摘要: Estrogens, which have been associated with several types of human and animal cancers, can induce tumor angiogenesis in the pituitary Fischer 344 rats. The mechanistic details induction, during estrogen carcinogenesis, are still unknown. To elucidate role regulation female rats, density blood vessels was analysed using factor VIII related antigen (FVIIIRAg) immunohistochemistry expression vascular endothelial growth factor/vascular permeability (VEGF/VPF) examined by Western blot immunohistochemical analysis. VEGF receptor (VEGFR-2/Flk-1/KDR) also immunohistochemistry. results demonstrated that 17beta-estradiol (E2) induces neovascularization, as well enlargement after 7 days exposure. high angiogenic potential an elevated VEGF/VPF protein E2 exposed ovariectomized (OVEX) FVIIIRAg specific lectin (UEA1) binding studies, indicate elevation initially occurred both non-endothelial cells. After 15 exposure, expression, cell population, sharply declined restricted to vessels. function non-endothelial-derived is not clear. Furthermore, studies VEGFR-2 (flk-1/KDR), significantly cells microblood These findings suggest over its (VEGFR-2) may play important initial step induced rat pituitary.