Regulation of ATP Binding Cassette Transporter A1 and Sterol Regulatory Element by Trans Fatty Acids

2011 ◽  
Vol 51 ◽  
pp. S51
Author(s):  
Fei Shao
2011 ◽  
Vol 31 (4) ◽  
pp. 278-285 ◽  
Author(s):  
Chai Siah Ku ◽  
Heather E. Rasmussen ◽  
Youngki Park ◽  
Elliot D. Jesch ◽  
Jiyoung Lee

2004 ◽  
Vol 377 (3) ◽  
pp. 545-552 ◽  
Author(s):  
Shubha MURTHY ◽  
Ella BORN ◽  
Satya N. MATHUR ◽  
F. Jeffrey FIELD

The effect of fatty acids on LXR (liver X receptors)-mediated enhancement of ABCA1 (ATP-binding cassette transporter A1) expression and cholesterol efflux was investigated in human intestinal cells CaCo-2. LXR activation by T0901317 increased basolateral cholesterol efflux to lipoprotein particles isolated at a density of 1.21 g/ml or higher. Oleic and arachidonic acids attenuated the amount of cholesterol isolated from these particles. Stearic, linoleic and docosahexaenoic acids also decreased cholesterol efflux from basolateral membranes, with the polyunsaturated fatty acids being the most potent. Although oleic, arachidonic and docosahexaenoic acids modestly decreased ABCA1 mRNA levels in response to LXR activation, stearic and linoleic acids did not. Except for oleic acid, all fatty acids substantially attenuated an increase in ABCA1 mass secondary to LXR activation. Inhibiting acyl-CoA:cholesterol acyltransferase activity prevented the decrease in cholesterol efflux caused by oleic acid. Thus, in response to LXR activation, all fatty acids decreased the efflux of cholesterol from the basolateral membrane of CaCo-2 cells. Although modest suppression of ABCA1 gene expression by oleic, arachidonic and docosahexaenoic acids cannot be completely excluded as a mechanism, the predominant effect of fatty acids on ABCA1 expression and cholesterol efflux is at a post-transcriptional level.


2018 ◽  
Vol 24 (26) ◽  
pp. 3123-3131 ◽  
Author(s):  
Sajedeh Gholipour ◽  
Robert D. E. Sewell ◽  
Zahra Lorigooini ◽  
Mahmoud Rafieian-Kopaei

Atherosclerosis is an inflammatory vascular disease that is characterized by progressive accumulation of cholesterol in the arterial walls and it is a major cause of cardiovascular disease. Issues related to the side effects of synthetic drugs have in recent times, led to the misuse of drugs, a lack of patient consultations, and consequently, a disruption in meticulous disease control. Therefore, a new insight into medicinal plants has recently emerged and much research has been conducted on these herbs in an attempt to prepare novel naturally based drugs. The aim of this review article was to scrutinize the molecular mechanisms of medicinal plants possessing effectiveness against atherosclerosis. To conduct the review, electronic searches were performed to retrieve potentially relevant publications, indexed within internet databases and reference textbooks concerning the effects and underlying molecular mechanisms of plants or their constituents used to treat atherosclerosis. Overall, medicinal plants facilitate atherosclerosis treatment through a variety of mechanisms which include the regulation of expression of inflammatory factors, stimulation of peroxisome proliferator-activated receptors (PPARs), inhibition of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMG-CoA reductase), promotion of ATP-binding cassette transporter A1 (ABCA1) as well as ATP-binding cassette transporter G (ABCG), facilitation of adiponectin activity, reduction of sterol regulatory element-binding proteins (SREBPs) and antioxidant activity. An increased perception of these herbal mechanistic links is an important prelude to the design of novel plant based drugs.


Diabetes ◽  
2002 ◽  
Vol 51 (10) ◽  
pp. 2922-2928 ◽  
Author(s):  
Y. Uehara ◽  
T. Engel ◽  
Z. Li ◽  
C. Goepfert ◽  
S. Rust ◽  
...  

2007 ◽  
Vol 191 (1) ◽  
pp. 11-21 ◽  
Author(s):  
Yoshinari Uehara ◽  
Shin-ichiro Miura ◽  
Arnold von Eckardstein ◽  
Satomi Abe ◽  
Akihiro Fujii ◽  
...  

1997 ◽  
Vol 249 (3) ◽  
pp. 657-661 ◽  
Author(s):  
Nicolette Verleur ◽  
Ewald H. Hettema ◽  
Carlo W. T. Roermund ◽  
Henk F. Tabak ◽  
Ronald J. A. Wanders

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