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J. Biol. Chem., Vol. 277, Issue 35, 32063-32070, August 30, 2002
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From the Abnormal vascular smooth muscle cell (VSMC)
proliferation is a key feature of atherosclerosis and restenosis;
however, the mechanisms regulating growth remain unclear. Herein we
show that inhibition of the aldehyde-metabolizing enzyme aldose
reductase (AR) inhibits NF-
Aldose Reductase Mediates Mitogenic Signaling in Vascular Smooth
Muscle Cells*
,,
Department of Human Biological Chemistry and
Genetics, University of Texas Medical Branch, Galveston, Texas
77555, the § Division of Cardiology, Department of Medicine,
University of Louisville, Louisville, Kentucky 40402, and the
¶ Cytokine Research Laboratory, the Department of
Bioimmunotherapy, University of Texas M. D. Anderson Cancer
Center, Houston, Texas 77030
B activation during restenosis of
balloon-injured rat carotid arteries as well as VSMC proliferation due
to tumor necrosis factor 
(TNF-) stimulation. Inhibition of VSMC
growth by AR inhibitors was not accompanied by increase in cell death or apoptosis. Inhibition of AR led to a decrease in the activity of the
transcription factor NF-B in culture and in the neointima of rat
carotid arteries after balloon injury. Inhibition of AR in VSMC also
prevented the activation of NF-B by basic fibroblast growth factor
(bFGF), angiotensin-II (Ang-II), and platelet-derived growth factor
(PDGF-AB). The VSMC treated with AR inhibitors showed decreased nuclear
translocation of NF-B and diminished phosphorylation and proteolytic
degradation of IB-. Under identical conditions, treatment with AR
inhibitors also prevented the activation of protein kinase C (PKC) by
TNF-, bFGF, Ang-II, and PDGF-AB but not phorbol esters, indicating
that AR inhibitors prevent PKC stimulation or the availability of its
activator but not PKC itself. Treatment with antisense AR, which
decreased the AR activity by >80%, attenuated PKC activation in
TNF-, bFGF, Ang-II, and PDGF-AB-stimulated VSMC and prevented
TNF--induced proliferation. Collectively, these data suggest that
inhibition of NF-B may be a significant cause of the antimitogenic
effects of AR inhibition and that this may be related to disruption of
PKC-associated signaling in the AR-inhibited cells.
*
This work was supported in part by National Institutes of
Health Grants DK 36118, HL55477, and HL59378.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: Dept. of Human
Biological Chemistry and Genetics, Rm. 6.644, Basic Science Bldg., University of Texas Medical Branch, Galveston, TX 77555-0647. Tel.:
409-772-3926; Fax: 409-772-9679; E-mail: ssrivast@utmb.edu.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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