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J Biol Chem, Vol. 275, Issue 2, 883-889, January 14, 2000
From the Eisai Co. Ltd., Tsukuba Research Laboratories,
Tokodai 5-1-3, Tsukuba, Ibaraki 300-2635, Japan
Proliferation of vascular smooth muscle cells
(SMC) is a crucial event in the formation of atherosclerotic tissues
and is regulated by nuclear transcriptional factors including nuclear factor-
Regulation of Vascular Smooth Muscle Cell Proliferation by
Nuclear Factor-
B and Its Inhibitor, I-B*
,
B (NF-B). We constructed a reporter gene assay to measure NF-B-dependent transcriptional activity in SMC. Thrombin
receptor-activating peptide (TRAP) and basic fibroblast growth factor
(bFGF) stimulated SMC proliferation and rapidly enhanced the NF-B
transcriptional activity in a dose-dependent manner.
4-Cyano-5,5-bis-(methoxyphenyl)4-pentenoic acid (E5510) significantly
inhibited SMC proliferation and also suppressed NF-B transcription
stimulated by TRAP and bFGF. In contrast, although tumor necrosis
factor (TNF)-
activated NF-B transcription, E5510 had no effect
on TNF--induced activation. NF-B was activated after the
stimulation of TRAP, bFGF, and TNF- in electrophoretic mobility
shift assay, and E5510 suppressed the NF-B activation induced by
TRAP and bFGF but not the activation by TNF-. Western blot analysis
of I-B and I-B
, inhibitors of NF-B, indicated that
I-B degradation, rather than I-B degradation, was important
in NF-B activation after the stimulation of TRAP and bFGF. PD98059,
an inhibitor of extracellular signal-regulated kinase (ERK) kinase,
suppressed NF-B transcriptional activity and SMC proliferation. The
phosphorylation of ERK1/2 was rapidly induced by TRAP and bFGF but not
by TNF-. These results indicate that TRAP and bFGF induced I-B
degradation and NF-B activation through a distinct pathway from
TNF- and that ERK1/2 may play an important role in NF-B
activation induced by TRAP and bFGF.
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Tel: 81-298-47-5809;
Fax: 81-298-47-2037; E-mail: m-hoshi@hhc.eisai.co.jp.
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