Angiotensin II augments advanced glycation end product‐induced pericyte apoptosis through RAGE overexpression
2005; Wiley; Volume: 579; Issue: 20 Linguagem: Inglês
10.1016/j.febslet.2005.06.058
ISSN1873-3468
AutoresSho‐ichi Yamagishi, Masayoshi Takeuchi, Takanori Matsui, Kazuo Nakamura, Tsutomu Imaizumi, Hiroyoshi Inoue,
Tópico(s)Neurological Disease Mechanisms and Treatments
ResumoAdvanced 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.
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