(Circulation. 1997;96:2361-2367.)
© 1997 American Heart Association, Inc.
Articles |
Platelet-Derived Growth Factor–Stimulated Superoxide Anion Production Modulates Activation of Transcription Factor NF-
B and Expression of Monocyte Chemoattractant Protein 1 in Human Aortic Smooth Muscle Cells
From the Zentrum der Physiologie, Klinikum der Johann Wolfgang Goethe Universität, Frankfurt am Main, Germany.
Correspondence to Takeshi Marumo, MD, PhD, Zentrum der Physiologie, Klinikum der Johann Wolfgang Goethe Universität, Theodor-Stern-Kai 7, D-60590 Frankfurt am Main, Germany. E-mail busse{at}merlin.add.uni-frankfurt.de
Background Platelet-derived growth factor (PDGF)
and superoxide anion (O2·-) have been
implicated in vascular diseases. We investigated whether PDGF
stimulates the production of O2·- in
human aortic smooth muscle cells (HSMCs) and whether
O2·- leads in this way to the activation of
nuclear factor–B (NF-B) and induction of monocyte
chemoattractant protein 1 (MCP-1) in PDGF-stimulated HSMCs.
Methods and Results PDGF-AB concentration- and
time-dependently stimulated O2·- generation
from HSMCs. The stimulatory effect of PDGF-AB was mimicked by PDGF-BB
but not by PDGF-AA. The generation of O2·-
by PDGF-AB was attenuated by the NAD(P)H oxidase inhibitor
iodonium diphenyl, the specific protein kinase C (PKC)
inhibitor Ro 31-8220, and the phosphatidylinositol 3-kinase
inhibitor wortmannin. Allopurinol and
nifedipine had no effect on PDGF-AB–induced
O2·- release, whereas
indomethacin potentiated this response. Gel mobility
shift assay revealed that PDGF-AB increased the binding activity of
NF-B, which contained predominantly the p50/p65 heterodimer in
nuclear extracts from HSMCs. Superoxide dismutase as well as iodonium
diphenyl, Ro 31-8220, and wortmannin attenuated PDGF-AB–induced
activation of NF-B and expression of MCP-1 mRNA. In contrast,
superoxide dismutase did not inhibit the interleukin-1ß–induced
NF-B activation.
Conclusions The results demonstrate that PDGF
stimulates O2·- generation in HSMCs via
PKC-dependent and wortmannin-sensitive pathways involving
flavoenzyme(s). This PDGF-induced O2·-
production may be involved in vascular lesion formation by
mediating, at least in part, NF-B activation and MCP-1 induction.
Key Words: growth substances • atherosclerosis • lesion
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