ABCA1
泡沫电池
CD36
过氧化物酶体增殖物激活受体
核受体
ATP结合盒传送带1
丹吉尔病
肝X受体
胆固醇逆向转运
受体
脂质代谢
生物
胆固醇
氧甾醇
细胞生物学
清道夫受体
化学
内分泌学
生物化学
脂蛋白
转录因子
运输机
基因
作者
Giulia Chinetti-Gbaguidi,Sophie Lestavel,Bocher,Remaley At,Bernadette Neve,IP Torra,Elisabeth Teissier,Anne Minnich,Michael Jaye,Nicholas Duverger,Brewer Hb,Fruchart Jc,Clavey,Bart Staels
出处
期刊:Nature Medicine
[Springer Nature]
日期:2001-01-01
卷期号:7 (1): 53-58
被引量:1088
摘要
Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors that regulate lipid and glucose metabolism and cellular differentiation. PPAR-alpha and PPAR-gamma are both expressed in human macrophages where they exert anti-inflammatory effects. The activation of PPAR-alpha may promote foam-cell formation by inducing expression of the macrophage scavenger receptor CD36. This prompted us to investigate the influence of different PPAR-activators on cholesterol metabolism and foam-cell formation of human primary and THP-1 macrophages. Here we show that PPAR-alpha and PPAR-gamma activators do not influence acetylated low density lipoprotein-induced foam-cell formation of human macrophages. In contrast, PPAR-alpha and PPAR-gamma activators induce the expression of the gene encoding ABCA1, a transporter that controls apoAI-mediated cholesterol efflux from macrophages. These effects are likely due to enhanced expression of liver-x-receptor alpha, an oxysterol-activated nuclear receptor which induces ABCA1-promoter transcription. Moreover, PPAR-alpha and PPAR-gamma activators increase apoAI-induced cholesterol efflux from normal macrophages. In contrast, PPAR-alpha or PPAR-gamma activation does not influence cholesterol efflux from macrophages isolated from patients with Tangier disease, which is due to a genetic defect in ABCA1. Here we identify a regulatory role for PPAR-alpha and PPAR-gamma in the first steps of the reverse-cholesterol-transport pathway through the activation of ABCA1-mediated cholesterol efflux in human macrophages.
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