VEGF release by retinal glia depends on both oxygen and glucose supply

Isolated retinae or isolated Muller cells were cultured in vitro, and vascular endothelial growth factor (VEGF) was assayed as protein (by ELISA) and as mRNA (by semi-quantitative RT-PCR). In both types of cultures, hypoxia (5% O-2) resulted in an upregulated VEGF release. While the unstimulated VEGF secretion was virtually independent of glucose (0.125-25 mM), elevated glucose concentrations (10-25 mM) blocked most of the stimulatory effect of hypoxia on VEGF mRNA synthesis (determined in Muller cell cultures) as well as on VEGF release (in both retina and Muller cell cultures). It is concluded that in retinal glial (Muller) cells, being responsible for retinal VEGF synthesis (and, thus, for undesirable neovascularization), the metabolic effects of hypoxia can be compensated by a surplus of glucose. NeuroReport 11:3533-3537 (C) 2000 Lippincott Williams & Wilkins.