Regulation of MSR-1 and CD36 in macrophages by LOX-1 mediated through PPAR-¦Ã

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• 作者：Yao Dai ; Wei Su ; Zufeng Ding ; Xianwei Wang ; Federico Mercanti ; Mingwei Chen ; Sameer Raina ; Jawahar L. Mehta ; ^{MehtaJL@UAMS.edu}
• 关键词：Ox-LDL ; oxidized low density lipoprotein ; LOX-1 ; lectin-like scavenger receptor for ox-LDL ; MSR1 ; macrophage scavenger receptor 1 ; PPAR-¦Ã ; peroxisome proliferator-activated receptor gamma ; LOX-1 KO ; LOX-1 Knockout ; Dil-ox-LDL ; 1 ; 1&prime ; -dioctadecyl-3 ; 3
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2013
• 出版时间：15 February, 2013
• 年：2013
• 卷：431
• 期：3
• 页码：496-500
• 全文大小：704 K

文摘

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-¦Ã in LOX-1 KO macrophages. To ascertain the role of PPAR-¦Ã in the altered expression of MSR1 and CD36, LOX-1 KO macrophages were treated with troglitazone, a PPAR-¦Ã agonist. Activation of PPAR-¦Ã 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-¦Ã.