Document Detail


Olmesartan blocks advanced glycation end products (AGEs)-induced angiogenesis in vitro by suppressing receptor for AGEs (RAGE) expression.
MedLine Citation:
PMID:  17560613     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-05-18
Journal Detail:
Title:  Microvascular research     Volume:  75     ISSN:  0026-2862     ISO Abbreviation:  Microvasc. Res.     Publication Date:  2008 Jan 
Date Detail:
Created Date:  2007-12-24     Completed Date:  2008-03-20     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0165035     Medline TA:  Microvasc Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  130-4     Citation Subset:  IM    
Affiliation:
Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume 830-0011, Japan. shoichi@med.kurume-u.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Angiogenesis Inhibitors / 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:
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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