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Licensed Unlicensed Requires Authentication Published by De Gruyter October 10, 2007

The −374A allele of the receptor for advanced glycation end products (RAGE) gene promoter is a protective factor against cardiovascular lesions in type 2 diabetes mellitus patients

  • Geraldo Picheth , Costantino O. Costantini , Fábio O. Pedrosa , Tania Leme da Rocha Martinez and Emanuel Maltempi de Souza
From the journal


Background: Polymorphisms of the receptor for advanced glycation end products (RAGE) gene have been associated with diabetes, coronary artery disease (CAD) and inflammatory processes. The –374T>A RAGE gene promoter polymorphism was shown to affect gene transcription. The aim of this study was to evaluate the association of the –374T>A polymorphism with the severity of CAD in patients with or without type 2 diabetes mellitus.

Methods: We studied 246 Euro-Brazilians with angiographically defined CAD (stenosis >50%), comprising type 2 diabetic (n=98) and non-diabetic subjects (n=148). Genotyping was performed by PCR-restriction fragment length polymorphism using Tsp509I restriction enzyme.

Results: The AA genotype was associated with a significant decrease in CAD severity estimated by the number of diseased vessels (1.43±0.5 vs. 2.49±1.1; p=0.002) and the Duke score (27.3±10.8 vs. 49.3±20.1; p=0.001) only in the group of CAD subjects with type 2 diabetes mellitus. The protective effect of the AA genotype against severity of CAD was not observed in the non-diabetic group.

Conclusion: This result confirms that the –374AA genotype of the RAGE gene promoter is a protective factor against the severity of CAD lesions in type 2 diabetic patients.

Clin Chem Lab Med 2007;45:1268–72.

Corresponding author: Geraldo Picheth, Department of Biochemistry and Molecular Biology, Federal University of Paraná, P.O. Box 19046, 81531-990 Curitiba, PR, Brazil Phone/Fax: +55-41-3274-5593, ,

Received: 2007-1-12
Accepted: 2007-6-1
Published Online: 2007-10-10
Published in Print: 2007-10-01

©2007 by Walter de Gruyter Berlin New York

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