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Papers In Press, published online ahead of print April 16, 2003
J. Lipid Res., doi:10.1194/jlr.M300077-JLR200
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Medicine Dept., University of Alabama at Birmingham, Birmingham, AL 35294-0012
Corresponding Author: wbradley{at}uab.edu
Certain triglyceride-rich lipoproteins (TRL), specifically, chylomicrons, dyslipemic very low-density lipoproteins, and their remnants, are atherogenic and can induce monocyte-macrophage foam cell formation in vitro via the apolipoprotein B48 receptor (apoB48R). Human atherosclerotic lesion foam cells express the apoB48R, as determined immunohistochemically, suggesting it can play a role in the conversion of macrophages into foam cells in vivo. The regulation of the apoB48R in monocyte-macrophages is not fully understood albeit previous studies indicated that cellular sterol levels and state of differentiation do not affect apoB48R expression. Since peroxisome proliferator activated receptors (PPAR) regulate some aspects of cellular lipid metabolism and may be protective in atherogenesis by upregulation of LXR
Revised on March 21, 2003
Accepted on April 2, 2003
PPAR
and PPAR
activators suppress the monocyte-macrophage apolipoprotein B48 receptor
and ABCA1, we examined the regulation of apoB48R by PPAR ligands in human monocyte-macrophages. Using real-time PCR, Northern, Western, and functional cellular lipid accumulation assays, we show that PPAR and PPAR
activators significantly suppress the expression of apoB48R mRNA in human THP-1 and blood-borne monocyte-macrophages. Moreover, PPAR activators inhibit the expression of the apoB48R protein and, notably, the apoB48R-mediated lipid accumulation of TRL by THP-1 monocytes in vitro. If PPAR activators also suppress the apoB48R pathway in vivo, diminished apoB48R-mediated monocyte-macrophage lipid accumulation may be yet another anti-atherogenic effect of the action of PPAR ligands.
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