Role of the hepatic ABCA1 transporter in modulating intrahepatic cholesterol and plasma HDL cholesterol concentrations
Journal of Lipid Research, ISSN: 0022-2275, Vol: 44, Issue: 2, Page: 296-302
2003
- 209Citations
- 67Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations209
- Citation Indexes209
- 209
- CrossRef175
- Captures67
- Readers67
- 67
Article Description
The current model for reverse cholesterol transport proposes that HDL transports excess cholesterol derived primarily from peripheral cells to the liver for removal. However, recent studies in ABCA1 transgenic mice suggest that the liver itself may be a major source of HDL cholesterol (HDL-C). To directly investigate the hepatic contribution to plasma HDL-C levels, we generated an adenovirus (rABCA1-GFP-AdV) that targets expression of mouse ABCA1-GFP in vivo to the liver. Compared with mice injected with control AdV, infusion of rABCA1-GFP-AdV into C57Bl/6 mice resulted in increased expression of mouse ABCA1 mRNA and protein in the liver. ApoA-I-dependent cholesterol efflux was increased 2.6-fold in primary hepatocytes isolated 1 day after rABCA1-GFP-AdV infusion. Hepatic ABCA1 expression in C57Bl/6 mice (n = 15) raised baseline levels of TC, PL, FC, HDL-C, apoE, and apoA-I by 150–300% ( P < 0.05 all). ABCA1 expression led to significant compensatory changes in expression of genes that increase hepatic cholesterol, including HMG-CoA reductase (3.5-fold), LDLr (2.1-fold), and LRP (5-fold) in the liver. These combined results demonstrate that ABCA1 plays a key role in hepatic cholesterol efflux, inducing pathways that modulate cholesterol homeostasis in the liver, and establish the liver as a major source of plasma HDL-C.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0022227520312165; http://dx.doi.org/10.1194/jlr.m200414-jlr200; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=10744222520&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/12576511; https://linkinghub.elsevier.com/retrieve/pii/S0022227520312165; http://www.jlr.org/lookup/doi/10.1194/jlr.M200414-JLR200; https://syndication.highwire.org/content/doi/10.1194/jlr.M200414-JLR200; https://dx.doi.org/10.1194/jlr.m200414-jlr200
Elsevier BV
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