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-kappaB 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.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Angiotensin II / pharmacology*
-
Angiotensin II Type 1 Receptor Blockers / pharmacology
-
Animals
-
Apoptosis*
-
Benzimidazoles / pharmacology
-
Benzoates / pharmacology
-
Cells, Cultured
-
Diabetic Retinopathy / metabolism
-
Glycation End Products, Advanced / toxicity*
-
NF-kappa B / genetics
-
NF-kappa B / metabolism
-
Pericytes / drug effects
-
Pericytes / metabolism*
-
Promoter Regions, Genetic / genetics
-
RNA, Messenger / metabolism
-
Rats
-
Rats, Inbred SHR
-
Reactive Oxygen Species / metabolism
-
Receptor for Advanced Glycation End Products
-
Receptor, Angiotensin, Type 1 / metabolism*
-
Receptors, Immunologic
-
Retina / cytology
-
Telmisartan
-
Up-Regulation
Substances
-
Angiotensin II Type 1 Receptor Blockers
-
Benzimidazoles
-
Benzoates
-
Glycation End Products, Advanced
-
NF-kappa B
-
RNA, Messenger
-
Reactive Oxygen Species
-
Receptor for Advanced Glycation End Products
-
Receptor, Angiotensin, Type 1
-
Receptors, Immunologic
-
Angiotensin II
-
Telmisartan