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Published in: Inflammation 5/2012

01-10-2012

The Transcription Levels of ABCA1, ABCG1 and SR-BI are Negatively Associated with Plasma CRP in Chinese Populations with Various Risk Factors for Atherosclerosis

Authors: Chengjiang Li, Renyong Guo, Juanya Lou, Huali Zhou

Published in: Inflammation | Issue 5/2012

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Abstract

ATP binding cassette transporters (ABCA1, ABCG1) and scavenger receptor class B type I (SR-BI) are the three most important cellular cholesterol transporters that may prevent atherogenesis. The aim of this study was to investigate whether they were altered in Chinese populations with various risk factors for atherosclerosis and their potential associations with C-reactive protein (CRP). Healthy female controls (n = 30) and populations with various risk factors for atherosclerosis, such as type 2 diabetes (n = 17), hypertension (n = 12), overweight/obesity (n = 10), incipient nephropathy (n = 10), postmenopausal women (n = 9), male (n = 19), ageing male (n = 22), or smoking (n = 16), were recruited. ABCA1, ABCG1 and SR-BI mRNA levels in peripheral monocytes was determined. ABCG1 was decreased in all the risk populations except ageing. ABCA1 was decreased in all the risk populations except diabetes and male. SR-BI was decreased in those with overweight/obesity and incipient nephropathy. Circulating CRP was increased almost in all the risk populations except in males. The levels of ABCA1, ABCG1 and SR-BI were reduced in those with subclinically high CRP, and negatively associated with CRP level. These data indicates that ABCA1, ABCG1, and SR-BI are reduced in various populations under subclinically inflammatory conditions, which may potentially lead to impairing reverse cholesterol transport and developing atherosclerosis.
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Metadata
Title
The Transcription Levels of ABCA1, ABCG1 and SR-BI are Negatively Associated with Plasma CRP in Chinese Populations with Various Risk Factors for Atherosclerosis
Authors
Chengjiang Li
Renyong Guo
Juanya Lou
Huali Zhou
Publication date
01-10-2012
Publisher
Springer US
Published in
Inflammation / Issue 5/2012
Print ISSN: 0360-3997
Electronic ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-012-9479-9

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