| Olmesartan blocks advanced glycation end products (AGEs)-induced angiogenesis in vitro by suppressing receptor for AGEs (RAGE) expression. | |
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MedLine Citation:
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PMID: 17560613 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We have previously shown that advanced glycation end products (AGEs)-their receptor (RAGE) interaction elicits angiogenesis through autocrine production of vascular endothelial growth factor (VEGF), thus suggesting the active involvement of the AGEs-RAGE system in proliferative diabetic retinopathy (PDR). Since the crosstalk between the AGEs-RAGE and the renin-angiotensin system has also been proposed in the pathogenesis of PDR, we investigated here whether olmesartan, an angiotensin II type 1 receptor blocker, inhibited the AGEs-elicited angiogenesis in vitro by suppressing the NF-kappaB-mediated RAGE expression. Olmesartan significantly inhibited the AGEs-induced NF-kappaB promoter activity and RAGE gene expression in cultured microvascular endothelial cells (ECs). Further, olmesartan was found to block the AGEs-induced up-regulation of VEGF mRNA levels and consequent increase in DNA synthesis in ECs. These results demonstrated for the first time that olmesartan inhibited the AGEs signaling to angiogenesis by suppressing RAGE expression in ECs. Our present study suggests that blockade of the renin-angiotensin system by olmesartan may play a protective role against PDR by attenuating the deleterious effects of AGEs via down-regulation of RAGE. |
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Authors:
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Sho-ichi Yamagishi; Takanori Matsui; Kazuo Nakamura; Hiroyoshi Inoue; Masayoshi Takeuchi; Seiji Ueda; Kei Fukami; Seiya Okuda; Tsutomu Imaizumi |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2007-05-18 |
Journal Detail:
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Title: Microvascular research Volume: 75 ISSN: 0026-2862 ISO Abbreviation: Microvasc. Res. Publication Date: 2008 Jan |
Date Detail:
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Created Date: 2007-12-24 Completed Date: 2008-03-20 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 0165035 Medline TA: Microvasc Res Country: United States |
Other Details:
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Languages: eng Pagination: 130-4 Citation Subset: IM |
Affiliation:
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Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume 830-0011, Japan. shoichi@med.kurume-u.ac.jp |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Angiogenesis Inhibitors
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pharmacology*,
therapeutic use Angiotensin II Type 1 Receptor Blockers / pharmacology*, therapeutic use Cells, Cultured DNA Replication / drug effects Diabetic Retinopathy / metabolism, prevention & control Down-Regulation Endothelial Cells / drug effects*, metabolism Glycosylation End Products, Advanced / metabolism* Humans Imidazoles / pharmacology*, therapeutic use NF-kappa B / genetics, metabolism Neovascularization, Pathologic / genetics, metabolism, prevention & control* Promoter Regions, Genetic RNA, Messenger / metabolism Receptors, Immunologic / genetics, metabolism* Research Design Tetrazoles / pharmacology*, therapeutic use Transfection Vascular Endothelial Growth Factor A / genetics, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Angiogenesis Inhibitors; 0/Angiotensin II Type 1 Receptor Blockers; 0/Glycosylation End Products, Advanced; 0/Imidazoles; 0/NF-kappa B; 0/RNA, Messenger; 0/Receptors, Immunologic; 0/Tetrazoles; 0/VEGFA protein, human; 0/Vascular Endothelial Growth Factor A; 0/advanced glycosylation end-product receptor; 0/olmesartan |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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