Overexpression of STARD3 in human monocyte/macrophages induces an anti-atherogenic lipid phenotype

Dysregulated macrophage cholesterol homoeostasis lies at the heart of early and developing atheroma, and removal of excess cholesterol from macrophage foam cells, by efficient transport mechanisms, is central to stabilization and regression of atherosclerotic lesions. The present study demonstrates that transient overexpression of STARD3 START StAR (steroidogenic acute regulatory protein)-related lipid transfer domain 3; also known as MLN64 (metastatic lymph node 64), an endosomal cholesterol transporter and member of the START family of lipid trafficking proteins, induces significant increases in macrophage ABCA1 (ATP-binding cassette transporter A1) mRNA and protein, enhances 3Hcholesterol efflux to apo (apolipoprotein) AI, and reduces biosynthesis of cholesterol, cholesteryl ester, fatty acids, triacylglycerol and phospholipids from 14Cacetate, compared with controls.