Transient ischemia and hypoxia rapidly induced maximum expression of VEGF mRNA within 30 minutes in rat hearts, which lasted at least 3 hours.
Transient ischemia and hypoxia rapidly induce VEGF mRNA expression in the heart, suggesting a mechanism for stimulating coronary collateral formation.
Vascular endothelial growth factor (VEGF or vascular permeability factor), a direct-acting, endothelial cell-specific mitogen, has been suggested to be involved in development and maintenance of vasculatures in tumor neovascularization and in normal tissues. To investigate possible roles of VEGF in ischemic hearts, we studied induction of VEGF mRNA by ischemia and hypoxia using coronary artery-ligated hearts in vivo and perfused hearts and cultured myocardial cells in vitro. VEGF mRNA was potently induced by ischemia in the heart in vivo. In perfused hearts, maximum expression was rapidly induced (within 30 min) by transient reversible ischemia (5-10 min of ischemia) and lasted at least 3 h. Induction was also caused by hypoxia, which was confirmed in perfused hearts and cultured myocardial cells. These results suggest that induction of VEGF mRNA is upregulated by oxygen deprivation in the heart and that not only infarction but also chronic ischemia in the clinical setting could induce VEGF as a potent angiogenesis factor to stimulate coronary collateral formation.
Hashimoto et al. (1994) studied Myocardial ischemia and hypoxia. Transient ischemia and hypoxia was evaluated on Induction of VEGF mRNA expression. Transient ischemia and hypoxia rapidly induced maximum expression of VEGF mRNA within 30 minutes in rat hearts, which lasted at least 3 hours.