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Vol. 293, Issue 3, 779-787, June 2000
Department of Pharmacology and Cell Biophysics, College of
Medicine, University of Cincinnati, Cincinnati, Ohio
Vascular endothelial growth factor (VEGF) is an endothelial cell
mitogen that promotes angiogenesis during embryonic development and the
progression of certain pathologies. This study examined the regulation
of VEGF expression by adenosine receptor (AR) activation in PC12 rat
pheochromocytoma cells. Treatment of cells with the AR agonist CGS21680
reduced the VEGF mRNA level to ~20% of that in control cells with an
EC50 value of 0.47 nM, indicative of mediation by the
A2AAR. Down-regulation of VEGF mRNA by CGS21680 was
abolished by pretreatment of cells with the AR antagonist ZM241385.
Additionally, ZM241385 alone increased VEGF mRNA by 2.8-fold above
basal. RNase protection assays indicated that CGS21680 down-regulated
VEGF121, VEGF165, and VEGF189
transcripts. VEGF protein secretion was similarly decreased by
CGS21680. Under hypoxic conditions, VEGF mRNA expression was reduced by
85.7% after pretreatment with CGS21680. The down-regulation response
appears to be mediated predominately by coupling of the
A2AAR to Gs because cholera toxin treatment
also reduced VEGF expression. The decrease in VEGF mRNA steady-state
levels after A2AAR activation is apparently due to a
decrease in the VEGF gene transcription rate and not to a decrease in
mRNA stability. Thus, depending on the cell type, adenosine may have an
inhibitory effect on VEGF production, which may have implications in
blood vessel development.
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