Differential regulation of the STARD1 subfamily of START lipid trafficking proteins in human macrophages

被引：31

作者：

Borthwick, Faye ^{[1
]}

Taylor, Janice M. ^{[1
]}

Bartholomew, Chris ^{[2
]}

Graham, Annette ^{[1
]}

机构：

[1] Glasgow Caledonian Univ, Vasc Biol Grp, Glasgow G4 0BA, Lanark, Scotland

[2] Glasgow Caledonian Univ, Dept Biol & Biomed Sci, Glasgow G4 0BA, Lanark, Scotland

来源：

FEBS LETTERS | 2009年 / 583卷 / 07期

关键词：

Atherosclerosis; Macrophage; 'Foam cell'; Steroidogenic acute regulatory protein; (StAR/STARD1); STARD3/metastatic lymph node 64 (MLN64); Liver X receptor; Peroxisome proliferator activated receptor; Retinoic acid X receptor; Sterol regulatory element binding protein; CHOLESTEROL EFFLUX; MLN64; EXPRESSION; METABOLISM; MEDIATORS; LY295427; LDL;

D O I：

10.1016/j.febslet.2009.02.042

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

The STARD1 subfamily of 'START' lipid trafficking proteins can reduce macrophage lipid content and inflammatory status (STARD1; StAR), and traffic cholesterol from endosomes (STARD3/MLN64). During macrophage differentiation, STARD1 mRNA and protein increase with sterol content, while the reverse is true for STARD3. Sterol depletion (methyl beta-cyclodextrin) enhances STARD3, and represses STARD1 expression. Agonists of Liver X receptors, peroxisome proliferator activated receptor-gamma and retinoic acid X receptors increase STARD1 expression, while hypocholesterolaemic agent, LY295427, reveals both STARD1 and STARD3 as putative SREBP-target genes. Pathophysiological 'foam cell' formation, induced by acetylated or oxidized LDL, significantly reduced both STARD1 and STARD3 gene expression. Differential regulation of STARD1 and D3 reflects their distinct roles in macrophage cholesterol metabolism, and may inform anti-atherogenic strategies. (C) 2009 Published by Elsevier B. V. on behalf of the Federation of European Biochemical Societies.

引用

页码：1147 / 1153

页数：7

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