Isolated retinae or isolated Muller cells were cultured in vitro, and vascu
lar 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 VEG
F secretion was virtually independent of glucose (0.125-25 mM), elevated gl
ucose concentrations (10-25 mM) blocked most of the stimulatory effect of h
ypoxia on VEGF mRNA synthesis (determined in Muller cell cultures) as well
as on VEGF release (in both retina and Muller cell cultures). It is conclud
ed that in retinal glial (Muller) cells, being responsible for retinal VEGF
synthesis (and, thus, for undesirable neovascularization), the metabolic e
ffects of hypoxia can be compensated by a surplus of glucose. NeuroReport 1
1:3533-3537 (C) 2000 Lippincott Williams & Wilkins.