PMID- 20491656
OWN - NLM
STAT- MEDLINE
DCOM- 20100916
LR  - 20211020
IS  - 1470-8736 (Electronic)
IS  - 0143-5221 (Print)
IS  - 0143-5221 (Linking)
VI  - 119
IP  - 7
DP  - 2010 Jun 22
TI  - Overexpression of STARD3 in human monocyte/macrophages induces an 
      anti-atherogenic lipid phenotype.
PG  - 265-72
LID - 10.1042/CS20100266 [doi]
AB  - 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 
      [(3)H]cholesterol efflux to apo (apolipoprotein) AI, and reduces biosynthesis of 
      cholesterol, cholesteryl ester, fatty acids, triacylglycerol and phospholipids 
      from [(14)C]acetate, compared with controls. Notably, overexpression of STARD3 
      prevents increases in cholesterol esterification in response to acetylated LDL 
      (low-density lipoprotein), blocking cholesteryl ester deposition. Thus enhanced 
      endosomal trafficking via STARD3 induces an anti-atherogenic macrophage lipid 
      phenotype, positing a potentially therapeutic strategy.
FAU - Borthwick, Faye
AU  - Borthwick F
AD  - Vascular Biology Group, Department of Biological and Biomedical Sciences, Glasgow 
      Caledonian University, Glasgow G4 0BA, UK.
FAU - Allen, Anne-Marie
AU  - Allen AM
FAU - Taylor, Janice M
AU  - Taylor JM
FAU - Graham, Annette
AU  - Graham A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100622
PL  - England
TA  - Clin Sci (Lond)
JT  - Clinical science (London, England : 1979)
JID - 7905731
RN  - 0 (Carrier Proteins)
RN  - 0 (Membrane Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (STARD3 protein, human)
SB  - IM
MH  - Aorta/metabolism
MH  - Atherosclerosis/*metabolism
MH  - Carrier Proteins/*biosynthesis/genetics
MH  - Cells, Cultured
MH  - Foam Cells/metabolism
MH  - Gene Expression Regulation/physiology
MH  - Humans
MH  - Lipid Metabolism/*physiology
MH  - Macrophages/*metabolism
MH  - Membrane Proteins/*biosynthesis/genetics
MH  - Monocytes/*metabolism
MH  - Phenotype
MH  - Polymerase Chain Reaction/methods
MH  - RNA, Messenger/genetics
PMC - PMC2891001
EDAT- 2010/05/25 06:00
MHDA- 2010/09/18 06:00
PMCR- 2010/06/22
CRDT- 2010/05/25 06:00
PHST- 2010/05/25 06:00 [entrez]
PHST- 2010/05/25 06:00 [pubmed]
PHST- 2010/09/18 06:00 [medline]
PHST- 2010/06/22 00:00 [pmc-release]
AID - CS20100266 [pii]
AID - cs1190265 [pii]
AID - 10.1042/CS20100266 [doi]
PST - epublish
SO  - Clin Sci (Lond). 2010 Jun 22;119(7):265-72. doi: 10.1042/CS20100266.