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J. Biol. Chem., Vol. 275, Issue 23, 17661-17670, June 9, 2000
From the Oxidative stress caused by phorbol esters or
reactive oxygen up-regulates the class A scavenger receptor (SR-A) in
human smooth muscle cells (SMC), which normally do not express this
receptor. The increase in SR-A expression correlates with activation of the redox-sensitive transcription factors activating protein-1 c-Jun
and CCAAT enhancer-binding protein
Class A Scavenger Receptor Up-regulation in Smooth Muscle Cells
by Oxidized Low Density Lipoprotein*
ENHANCEMENT BY CALCIUM FLUX AND CONCURRENT CYCLOOXYGENASE-2
UP-REGULATION*
§¶,
, and§**
Gladstone Institute of Cardiovascular
Disease, the § Cardiovascular Research Institute, and the
Departments of ¶ Pediatrics and ** Pathology, University of
California, San Francisco, California 94143
. Here we show that coincubation
of SMC with macrophages or oxidized low density lipoproteins (LDL) from
macrophage-conditioned medium activates these same regulatory pathways
and stimulates SR-A expression. The increased SR-A gene transcription
induced by cell-oxidized LDL up-regulated SR-A mRNA and increased
by 30-fold the uptake of acetyl LDL, a ligand for the SR-A.
Copper-oxidized LDL also increased SR-A receptor expression. Oxidized
LDL with a lipid peroxide level of 80-100 nmol/mg of LDL protein and
an electrophoretic mobility ~1.5 times that of native LDL exhibited
the greatest bioactivity. Inhibition of calcium flux suppressed SR-A
induction by oxidized LDL. Conversely, calcium ionophore greatly
enhanced SR-A up-regulation by oxidized LDL or other treatments that
promote intracellular oxidative stress. This enhancement was dependent
upon concurrent up-regulation of SMC cyclooxygenase-2 expression and
activity and was blocked by the cyclooxygenase-2 inhibitors NS-398 and
Resveratrol. In THP-1 cells, oxidized LDL induced
monocyte-to-macrophage differentiation and increased SR-A expression.
These findings support a role for mildly oxidized LDL in the redox
regulation of macrophage differentiation and SR-A expression and
suggest that increased vascular oxidative stress may contribute to the
formation of both SMC and macrophage foam cells.
*
This work was funded in part by National Institutes of
Health Program Project Grant HL-47660.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.
Present address: Dept. of Medicine, Stanford University,
Stanford, CA 94545.
To whom correspondence should be addressed: Gladstone Institute
of Cardiovascular Disease, P.O. Box 419100, San Francisco, CA
94141-9100. Tel.: 415-826-7500; Fax: 415-285-5632; E-mail: rpitas@gladstone.ucsf.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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