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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2007-10-1
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pubmed:abstractText |
The receptor for advanced glycation end products (RAGE) and the angiotensin II type I receptor (AT1R) have been separately linked to the pathogenesis of diabetic atherosclerosis. However, no prior study has addressed a linkage between RAGE and AT1R in diabetic atherogenesis. Therefore, we tested the hypothesis that upregulation of the ligand-RAGE axis via AT1R is an essential process underlying the disease. Diabetes was induced in apolipoprotein E-deficient (ApoE(-/-)) mice by streptozotocin, and diabetic mice were treated with AT1 receptor blocker (ARB) for 6 weeks. Diabetic ApoE(-/-) mice that were AT1R-deficient (ApoE(-/-)AT1aR(-/-)) were also investigated. In diabetic ApoE(-/-) mice, AT1R was found to increase within 1 week of diabetes induction, before ligand-RAGE pathway activation and other inflammatory changes were observed. Both ARB treatment and AT1aR deficiency suppressed diabetic atherosclerosis, ligand-RAGE expression and inflammatory changes. In contrast, upregulation of the ligand-RAGE pathway was noted in atherosclerotic plaques from non-diabetic ApoE(-/-) mice infused with angiotensin II. In cultured vascular smooth muscle cells, angiotensin II increased RAGE protein levels via AT1R stimulation. Upregulation of the ligand-RAGE pathway via AT1R is an essential mechanism in diabetic atherosclerosis, implying that ARB might decrease diabetic atherogenesis by inhibiting ligand-RAGE signals.
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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/Adaptor Proteins, Signal Transducing,
http://linkedlifedata.com/resource/pubmed/chemical/Agtrap protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II Type 1 Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins E,
http://linkedlifedata.com/resource/pubmed/chemical/Glycosylation End Products, Advanced,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/advanced glycosylation end-product...
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-2828
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pubmed:author |
pubmed-author:EgashiraKensukeK,
pubmed-author:HoriuchiMasatsuguM,
pubmed-author:IharaYoshikoY,
pubmed-author:IwaiMasaruM,
pubmed-author:KogaJun-ichiroJ,
pubmed-author:KuboMitsukiM,
pubmed-author:NakanoKakuK,
pubmed-author:OhtaniKishoK,
pubmed-author:SunagawaKenjiK,
pubmed-author:YamagishiSho-ichiS,
pubmed-author:ZhaoGangG
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pubmed:issnType |
Print
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pubmed:volume |
43
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
455-64
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pubmed:meshHeading |
pubmed-meshheading:17761193-Adaptor Proteins, Signal Transducing,
pubmed-meshheading:17761193-Angiotensin II Type 1 Receptor Blockers,
pubmed-meshheading:17761193-Animals,
pubmed-meshheading:17761193-Apolipoproteins E,
pubmed-meshheading:17761193-Blood Pressure,
pubmed-meshheading:17761193-Cell Proliferation,
pubmed-meshheading:17761193-Cells, Cultured,
pubmed-meshheading:17761193-Coronary Artery Disease,
pubmed-meshheading:17761193-Diabetes Mellitus, Experimental,
pubmed-meshheading:17761193-Diabetic Angiopathies,
pubmed-meshheading:17761193-Glycosylation End Products, Advanced,
pubmed-meshheading:17761193-Humans,
pubmed-meshheading:17761193-Male,
pubmed-meshheading:17761193-Mice,
pubmed-meshheading:17761193-Mice, Inbred C57BL,
pubmed-meshheading:17761193-Mice, Knockout,
pubmed-meshheading:17761193-Muscle, Smooth, Vascular,
pubmed-meshheading:17761193-Rats,
pubmed-meshheading:17761193-Receptors, Immunologic,
pubmed-meshheading:17761193-Renin-Angiotensin System,
pubmed-meshheading:17761193-Signal Transduction,
pubmed-meshheading:17761193-Up-Regulation
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pubmed:year |
2007
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pubmed:articleTitle |
Upregulation of the ligand-RAGE pathway via the angiotensin II type I receptor is essential in the pathogenesis of diabetic atherosclerosis.
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pubmed:affiliation |
Department of Cardiovascular Medicine, Graduate School of Medical Science, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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