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

Sho Ichi Yamagishi, Masayoshi Takeuchi, Takanori Matsui, Kazuo Nakamura, Tsutomu Imaizumi, Hiroyoshi Inoue

Research output: Contribution to journalArticlepeer-review

71 Citations (Scopus)

Abstract

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-κB 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.

Original languageEnglish
Pages (from-to)4265-4270
Number of pages6
JournalFEBS Letters
Volume579
Issue number20
DOIs
Publication statusPublished - 2005 Aug 15
Externally publishedYes

Keywords

  • Advanced glycation end products
  • Angiotensin II
  • Diabetic retinopathy
  • Oxidative stress
  • Pericyte loss
  • Receptor for AGEs

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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