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J Biol Chem, Vol. 275, Issue 2, 1241-1246, January 14, 2000
From the Department of Pathology and Center of Vascular Biology,
Weill Medical College of Cornell University,
New York, New York 10021
CD36, the macrophage type B scavenger
receptor, binds and internalizes oxidized low density lipoprotein, a
key event in the development of macrophage foam cells within
atherosclerotic lesions. Expression of CD36 in monocyte/macrophages is
dependent on differentiation status and exposure to soluble mediators.
In this study, we investigated the effect of transforming growth
factor-
Transforming Growth Factor-
1 (TGF-1) and TGF-2 Decrease
Expression of CD36, the Type B Scavenger Receptor, through
Mitogen-activated Protein Kinase Phosphorylation of Peroxisome
Proliferator-activated Receptor-
*
1 (TGF-1) and TGF-2 on the expression of CD36 in
macrophages. Treatment of phorbol ester-differentiated THP-1
macrophages with TGF-1 or TGF-2 significantly decreased
expression of CD36 mRNA and surface protein. TGF-1/TGF-2 also
inhibited CD36 mRNA expression induced by oxidized low density lipoprotein and 15-deoxy
12,14 prostaglandin
J2, a peroxisome proliferator-activated receptor (PPAR)-
ligand, suggesting that the TGF-1/TGF-2 down-regulated CD36
expression by inactivating PPAR--mediated signaling.
TGF-1/TGF-2 increased phosphorylation of both mitogen-activated
protein (MAP) kinase and PPAR-, whereas MAP kinase inhibitors
reversed suppression of CD36 and inhibited PPAR- phosphorylation
induced by TGF-1/TGF-2. Finally, MAP kinase inhibitors alone
increased expression of CD36 mRNA and surface protein but had no
effect on PPAR- protein levels. Our data demonstrate for the first
time that TGF-1 and TGF-2 decrease expression of CD36 by a
mechanism involving phosphorylation of MAP kinase, subsequent MAP
kinase phosphorylation of PPAR-, and a decrease in CD36 gene
transcription by phosphorylated PPAR-.
*
This work was supported by a Charles H. Revson and Norman
and Rosita Winston Foundation Postdoctoral Fellowship (to J. H.), National Institutes of Health SCOR Grant in Molecular Medicine and
Atherosclerosis P50-HL56987 (to A. C. N. and D. P. H.), and the
Abercrombie Foundation (to A. M. G.).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 Pathology,
A-626, Cornell University Medical College, 1300 York Ave., New York,
NY 10021. Tel.: 212-746-6470; Fax: 212-746-8789; E-mail: nicholso@mail.med.cornell.edu.
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