Role of formyl peptide receptor 2 on the serum amyloid A-induced macrophage foam cell formation

被引：28

作者：

Lee, Ha Young ^{[1
,2
]}

Kim, Sang Doo ^{[1
]}

Baek, Suk-Hwan ^{[3
]}

Choi, Joon Hyuk ^{[4
]}

Bae, Yoe-Sik ^{[1
,2
,5
]}

机构：

[1] Sungkyunkwan Univ, Dept Biol Sci, Suwon 440746, South Korea

[2] Dong A Univ, Mitochondria Hub Regulat Ctr, Pusan 602714, South Korea

[3] Yeungnam Univ, Coll Med, Dept Biochem & Mol Biol, Taegu 705717, South Korea

[4] Yeungnam Univ, Coll Med, Dept Pathol, Taegu 705717, South Korea

[5] Sungkyunkwan Univ, Samsung Adv Inst Hlth Sci & Technol, Seoul 135710, South Korea

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2013年 / 433卷 / 02期

基金：

新加坡国家研究基金会;

关键词：

Serum amyloid A; Formyl peptide receptor 2; Foam cell; Atherosclerosis; PROTEIN-COUPLED RECEPTOR; LOW-DENSITY-LIPOPROTEIN; CCL2; PRODUCTION; UP-REGULATION; HUMAN MONOCYTES; TNF-ALPHA; EXPRESSION; ATHEROSCLEROSIS; INFLAMMATION; ACTIVATION;

D O I：

10.1016/j.bbrc.2013.03.002

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Recently we demonstrated that SAA induces macrophage foam cell formation. In this study we show that SAA-induced foam cell formation is inhibited by formyl peptide receptor 2 (FPR2) antagonist WRW4, as well as by FPR2-targeted siRNA knockdown. SAA-stimulated LOX1 expression was also mediated by FPR2. We also found that SAA-stimulated foam cell formation and LOX1 expression was pertussis toxin-insensitive. In addition, FPR2 is upregulated in peripheral blood mononuclear cells from patients with atherosclerosis. Our findings therefore suggest that SAA stimulates foam cell formation via FPR2 signaling and LOX1 induction, and thus likely contributes to atherogenesis. (C) 2013 Elsevier Inc. All rights reserved.

引用

页码：255 / 259

页数：5

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