© 1997 American Heart Association, Inc.
Articles |
Nitric Oxide Promotes Proliferation and Plasminogen Activator Production by Coronary Venular Endothelium Through Endogenous bFGF
From the Department of Pharmacology (M.Z., A.P., F.L.), University of Florence (Italy); the Department of Biomedical Sciences and Biotechnologies (P.D., M.P.), University of Brescia (Italy); the Microcirculation Research Institute and Department of Medical Physiology (H.J.G.), Texas A&M University, College Station; and the Pharmacology Department (C.A.M.), A. Menarini Pharmaceuticals, Florence, Italy.
Correspondence to Marina Ziche, MD, Department of Pharmacology, University of Florence, Viale Morgagni 65, 50134 Florence, Italy. E-mail ziche{at}stat.ds.unifi.it
Abstract We reported previously that NO is responsible for
the angiogenesis produced by endothelium-dependent
vasodilating peptides. To investigate the mechanisms by which NO
controls angiogenesis, NO was assessed for the ability to affect cell
proliferation and upregulation of urokinase-type
plasminogen activator (uPA) induced by basic
fibroblast growth factor (bFGF) when added exogenously to or when
produced endogenously by coronary venular
endothelial cells (CVECs). The treatment of the cells
with the NO donor sodium nitroprusside (NaNp) induced uPA upregulation
and cell proliferation, which were prevented by anti-bFGF antibodies.
Similarly, the NO-dependent mitogenic activity of the
vasodilating peptide substance P (SP) was blocked by anti-bFGF
antibodies, thus implicating endogenous bFGF in the
NO-induced response. NaNp and SP induced bFGF expression as measured by
Western blot analysis of CVEC extracts and by differential
reverse transcriptase–polymerase chain reaction of bFGF mRNA.
SP-induced upregulation of bFGF was prevented by the NO synthase
inhibitor
N
-monomethyl-L-arginine.
We conclude that NO promotes cell proliferation and uPA upregulation in
CVECs by inducing endogenous bFGF and that this pathway
mediates the angiogenetic response to the vasoactive neuropeptide SP.
This signaling paradigm may provide an important link between shear
rate, NO, bFGF, and coronary angiogenesis.
Key Words: microvascular endothelium • plasminogen activator • autocrine proliferation • sodium nitroprusside • substance P
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