AGE-BSA decreases ABCG1 expression and reduces macrophage cholesterol efflux to HDL
Atherosclerosis, ISSN: 0021-9150, Vol: 192, Issue: 2, Page: 298-304
2007
- 50Citations
- 26Captures
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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
- Citations50
- Citation Indexes50
- 50
- CrossRef41
- Captures26
- Readers26
- 26
Article Description
Previous reports have suggested that advanced glycation end products (AGE) participate in the pathogenesis of diabetic macroangiopathy. However, current understanding of the mechanisms by which AGE may accelerate atherogenesis remains incomplete. Microarray and reverse transcription real-time PCR analyses revealed that exposure to AGE-BSA (BSA, bovine serum albumin) reduced mRNA levels (60%) in the ATP-binding cassette transporter G1 (ABCG1) but not ABCA1 in human macrophages. AGE-BSA also reduced ABCG1 protein levels. These effects occurred mainly through the receptor for AGE (RAGE), as an anti-RAGE antibody significantly limited ABCG1 mRNA reduction. Functional studies demonstrated that exposure to AGE-BSA decreased cholesterol efflux to high-density lipoprotein (HDL) ( P < 0.05) but not to apolipoprotein AI, compared to BSA treatment. Although liver X receptors (LXR) augment ABCG1 expression, macrophages treated with AGE-BSA showed no reduction in LXR mRNA levels or in the binding of nuclear proteins to the LXR response element, compared with BSA. Our data show that AGE-BSA can decrease cholesterol efflux from macrophages to HDL via an LXR-independent pathway. This novel mechanism may contribute to accelerated foam cell production and atherogenesis in diabetic patients.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S002191500600445X; http://dx.doi.org/10.1016/j.atherosclerosis.2006.07.023; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=34248156708&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/17005185; https://linkinghub.elsevier.com/retrieve/pii/S002191500600445X; https://dx.doi.org/10.1016/j.atherosclerosis.2006.07.023
Elsevier BV
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