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(Received for publication, January 15, 1997, and in revised form, April 3, 1997)
From the Departments of The proliferation of vascular endothelial cells
(EC) is an important event in angiogenesis. The synthesis of the EC
growth factor, vascular endothelial cell growth factor (VEGF), is
stimulated by a variety of activators; but the effects of important
vasoactive peptides are not well understood, and there are no known
natural inhibitors of VEGF production. We found that the vasoactive
peptides endothelin (ET)-1 and ET-3 stimulated the synthesis of VEGF
protein 3-4-fold in cultured human vascular smooth muscle cells,
comparable in magnitude to hypoxia. ET-1 and ET-3 acted through the ETA
and ETB receptors, respectively, and signaling through protein kinase C
was important. Atrial natriuretic peptide (ANP), C-type natriuretic peptide, and C-ANP-(4-23), a ligand for the natriuretic peptide clearance receptor, equipotently inhibited production of VEGF by as
much as 88% and inhibited ET- or hypoxia-stimulated VEGF transcription. EC proliferation and invasion of matrix were stimulated by VEGF secreted into the medium by ET-incubated vascular smooth muscle
cells. This was inhibited by ANP. Our results identify the natriuretic
peptides as the first peptide inhibitors of VEGF synthesis and indicate
a novel mechanism by which vasoactive peptides could modulate
angiogenesis.
Volume 272, Number 27,
Issue of July 4, 1997
pp. 17097-17103
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
§
,§
,§¶
and§¶
Medicine and
¶ Pharmacology, University of California, Irvine, California 92717 and the § Department of Veterans Affairs Medical Center,
Long Beach, California 90822
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