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Biochem Biophys Res Commun. 2013 Feb 15;431(3):496-500. doi: 10.1016/j.bbrc.2013.01.029. Epub 2013 Jan 16.

Regulation of MSR-1 and CD36 in macrophages by LOX-1 mediated through PPAR-γ.

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1
University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, AR 72212, USA.

Abstract

We observed uniform sustained Dil-ox-LDL uptake in macrophages in the presence or absence of ox-LDL receptor-1 (LOX-1). We wondered if the deficiency of LOX-1 modulates the expression of two other scavenger receptors, macrophage scavenger receptor-1 (MSR1) and CD36, on macrophages to account for the unaltered ox-LDL uptake. Macrophages were isolated from wild-type (WT) and LOX-1 knockout (KO) mice and stimulated with ox-LDL. Dil-ox-LDL uptake and expression of MSR1 and CD36 examined. Abrogation of LOX-1 did not significantly change Dil-ox-LDL uptake by macrophages. LOX-1 KO macrophages showed a significant decrease in CD36 at baseline as well as after ox-LDL stimulation and a marked almost 100% increase in the expression of MSR1, both at mRNA and protein levels (all p<0.05 vs. WT macrophages). Further, we observed a reduction in the expression of PPAR-γ in LOX-1 KO macrophages. To ascertain the role of PPAR-γ in the altered expression of MSR1 and CD36, LOX-1 KO macrophages were treated with troglitazone, a PPAR-γ agonist. Activation of PPAR-γ by troglitazone reversed the increased expression of MSR1 as well as the decreased expression of CD36 in LOX-1 KO macrophages. LOX-1 abrogation induces MSR1 and inhibits CD36 expression. The increase in MSR1 most likely accounts for sustained Dil-ox-LDL uptake despite LOX-1 abrogation. The alterations in CD36 and MSR1 occur through a decrease in PPAR-γ.

PMID:
23333385
DOI:
10.1016/j.bbrc.2013.01.029
[Indexed for MEDLINE]
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