Background information
Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) induces proliferation, migration, and fenestration in capillary endothelial cells derived from endocrine glands. EG-VEGF possesses an HIF-1 binding site; its expression is induced by hypoxia and restricted to the steroidogenic glands (ovary, testis, adrenal and placenta). Expression of EG-VEGF is often complementary to the expression of VEGF, suggesting that these molecules function in a coordinated manner. EG-VEGF is an example of a class of highly specific mitogens that act to regulate proliferation and differentiation of the vascular endothelium in a tissue-specific manner. It is expressed primarily in one type of tissue and acts selectively on one type of endothelium. EG-VEGF, possibly through binding to a G protein-coupled receptor, results in the activation of MAPK p44/42 and phosphatidylinositol 3-kinase signaling pathways, leading to proliferation, migration and survival of responsive endothelial cells .
