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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2007-5-24
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pubmed:abstractText |
High-density lipoprotein mediates a normal physiological process called reverse cholesterol transport. In this process, a scavenger receptor of the B class (SR-BI)/human homologue of SR-BI, CD36, and LIMPII analogous-1 (hSR-BI/CLA-1) facilitates the cellular uptake of cholesterol from high-density lipoprotein. In endothelial cells, high-density lipoprotein activates endothelial NO synthase via hSR-BI/CLA-1. Angiotensin II (Ang II) is a powerful accelerator of atherosclerosis and modulates the expression of endothelial NO synthase. In the present study, we have examined the role of Ang II on hSR-BI/CLA-1 expression in human umbilical vein endothelial cells. Our results showed that endogenous expression of hSR-BI/CLA-1 was suppressed by exposure to Ang II in human umbilical vein endothelial cells. Administration of the Ang II type-1 receptor blocker olmesartan inhibited Ang II-induced hSR-BI/CLA-1 protein repression. In Ang II-treated cells, high-density lipoprotein had no effect on endothelial NO synthase activation. Ang II decreased transcriptional activity of the hSR-BI/CLA-1 promoter. The inhibitory effect of Ang II on hSR-BI/CLA-1 promoter activity was abrogated by wortmannin and LY294002, specific inhibitors of phosphatidylinositol 3-kinase. Exposure of human umbilical vein endothelial cells to Ang II elicited a rapid phosphorylation of Akt and FoxO1, a known target of Akt signaling. Constitutively active Akt inhibits the activity of the hSR-BI/CLA-1 promoter, and a dominant-negative mutant of Akt or mutagenesis of a FoxO1 response element in the hSR-BI/CLA-1 abolished the ability of Ang II to suppress promoter activity. Together, these results indicate that the phosphatidylinositol 3-kinase/Akt/FoxO1 pathway participates in Ang II suppression of hSR-BI/CLA-1 expression and suggests that the endothelial receptor for hSR-BI/CLA-1 is downregulated by the renin-angiotensin system.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/2-(4-morpholinyl)-8-phenyl-4H-1-benz...,
http://linkedlifedata.com/resource/pubmed/chemical/Androstadienes,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Chromones,
http://linkedlifedata.com/resource/pubmed/chemical/FOXO1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Forkhead Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Imidazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Morpholines,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Oncogene Protein v-akt,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 1,
http://linkedlifedata.com/resource/pubmed/chemical/SCARB1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Scavenger Receptors, Class B,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrazoles,
http://linkedlifedata.com/resource/pubmed/chemical/olmesartan,
http://linkedlifedata.com/resource/pubmed/chemical/wortmannin
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1524-4563
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pubmed:author |
pubmed-author:AhmedRania A MRA,
pubmed-author:CaoWen-MingWM,
pubmed-author:ImachiHitomiH,
pubmed-author:IshidaToshihikoT,
pubmed-author:KosakaHiroakiH,
pubmed-author:LiJunhuaJ,
pubmed-author:MatsumotoKensukeK,
pubmed-author:MuraoKojiK,
pubmed-author:NishiuchiTakamasaT,
pubmed-author:UntermanTerry GTG,
pubmed-author:WongNorman C WNC,
pubmed-author:YuXiaoX
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pubmed:issnType |
Electronic
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pubmed:volume |
49
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1378-84
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:17404186-Androstadienes,
pubmed-meshheading:17404186-Angiotensin II,
pubmed-meshheading:17404186-Cells, Cultured,
pubmed-meshheading:17404186-Chromones,
pubmed-meshheading:17404186-Down-Regulation,
pubmed-meshheading:17404186-Endothelium, Vascular,
pubmed-meshheading:17404186-Forkhead Transcription Factors,
pubmed-meshheading:17404186-Gene Expression Regulation,
pubmed-meshheading:17404186-Humans,
pubmed-meshheading:17404186-Imidazoles,
pubmed-meshheading:17404186-Morpholines,
pubmed-meshheading:17404186-Nitric Oxide Synthase,
pubmed-meshheading:17404186-Oncogene Protein v-akt,
pubmed-meshheading:17404186-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:17404186-Phosphorylation,
pubmed-meshheading:17404186-Promoter Regions, Genetic,
pubmed-meshheading:17404186-RNA, Messenger,
pubmed-meshheading:17404186-Receptor, Angiotensin, Type 1,
pubmed-meshheading:17404186-Renin-Angiotensin System,
pubmed-meshheading:17404186-Scavenger Receptors, Class B,
pubmed-meshheading:17404186-Tetrazoles
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pubmed:year |
2007
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pubmed:articleTitle |
Regulation of scavenger receptor class BI gene expression by angiotensin II in vascular endothelial cells.
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pubmed:affiliation |
Division of Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, Kagawa University, 1750-1 Miki-cho, Kita-gun, Kagawa 761-0793, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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