Angiotensin II augments advanced glycation end product-induced pericyte apoptosis through RAGE overexpression

被引：74
作者：
Yamagishi, S
Takeuchi, M
Matsui, T
Nakamura, K
Imaizumi, T
Inoue, H
机构：
[1] Kurume Univ, Sch Med, Dept Internal Med 3, Kurume, Fukuoka 8300011, Japan
[2] Hokuriku Univ, Fac Pharmaceut Sci, Dept Pathophysiol Sci, Kanazawa, Ishikawa 9201181, Japan
[3] Kurume Univ, Sch Med, Radioisotope Inst Basic & Clin Med, Kurume, Fukuoka 8300011, Japan
来源：
FEBS LETTERS | 2005年 / 579卷 / 20期
关键词：
advanced glycation end products; angiotensin II; diabetic retinopathy; oxidative stress; pericyte loss; receptor for AGEs;
D O I：
10.1016/j.febslet.2005.06.058
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Advanced glycation end product (AGE)-their receptor (RAGE) and angiotensin II (AII) are implicated in diabetic retinopathy. However, a crosstalk between the two is not fully understood. In vivo, AGE injection stimulated RAGE expression in the eye of spontaneously hypertensive rats, which was blocked by an AII-type 1 receptor blocker, telmisartan. In vitro, AII-type 1 receptor-mediated reactive oxygen species generation elicited RAGE gene expression in pericytes through NF-kappa B activation. Further, AII augmented AGE-induced pericyte apoptosis, the earliest hallmark of diabetic retinopathy. Our present study may implicate a crosstalk between AGE-RAGE system and AII in diabetic retinopathy. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码：4265 / 4270
页数：6
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