Expression and Response to Hypoxia of Vascular Endothelial Growth Factor (VEGF) in Rat and Rabbit Tissues

VEGF is a potent and specific endothelial cell mitogen and an important regulator and inducer of angiogenesis. Recent finding of capillary budding in hypoxic rat brain suggested that hypoxia might initiate angiogenesis in brain. As a key factor of angiogenesis VEGF is thought to be potent in the basement membrane destruction and leakage. It can enhance microvascular permeability with a potency some 50,000 times that of histamine,11 which is likely to elicit hypoxic cerebral edema. The pathologic findings of cerebral thrombosis and petechial hemorrhages12 in high altitude cerebral edema are also consistent with VEGF physiological effects such as induction of thromboplastin activity5 and stimulation of von Willebrand factor release from endothelial cells.2 We surmise that VEGF may contribute to hihgh altitude cerebral edema (HACE). Here we report the expression and responce to hypoxia of VEGF mRNA, VEGF protein and its receptor (flt-1) in hypoxic tissues