Abstract:
: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.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Borthwick F,Taylor JM,Bartholomew C,Graham Adoi
10.1016/j.febslet.2009.02.042subject
Has Abstractpub_date
2009-04-02 00:00:00pages
1147-53issue
7eissn
0014-5793issn
1873-3468pii
S0014-5793(09)00173-2journal_volume
583pub_type
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