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Association between the AGTR1 polymorphism +1166A>C and serum levels of high-sensitivity C-reactive protein.

Journal article
Authors Petra Suchankova
Susanne Henningsson
Marie Olsson
Fariba Baghaei
Roland Rosmond
Göran Holm
Elias Eriksson
Agneta Ekman
Published in Regulatory peptides
Volume 152
Issue 1-3
Pages 28-32
ISSN 0167-0115
Publication year 2009
Published at Institute of Medicine
Institute of Neuroscience and Physiology, Department of Pharmacology
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 28-32
Language en
Links dx.doi.org/10.1016/j.regpep.2008.11...
Keywords AGTR1 polymorphism, serum levels, C-reactive protein
Subject categories Pharmacology and Toxicology

Abstract

Genetic factors have been shown to influence high-sensitivity C-reactive protein (hsCRP) levels, however, which genes that are involved in this process remains to be clarified. The renin-angiotensin system (RAS) is of importance for the regulation of inflammation, and blockade of angiotensin II type 1 receptors (AGTR1) influences hsCRP levels. These findings prompted us to investigate whether a polymorphism in the AGTR1 gene may influence hsCRP levels. Additionally, a polymorphism in the CRP gene that has previously been shown to influence hsCRP levels was genotyped. Serum levels of hsCRP were measured in 270 42-year-old women recruited from the population registry. Two single nucleotide polymorphisms were analysed: +1166A>C and +1444C>T of the AGTR1 and CRP gene, respectively. The A allele of the AGTR1 polymorphism +1166A>C was dose-dependently associated with higher hsCRP levels (p=0.014, adjusted for confounding factors and multiple comparisons). hsCRP levels were not significantly influenced by the CRP +1444C>T genotype; however, an interaction between the two studied polymorphisms with respect to hsCRP levels was observed (p=0.018). The significant association between the AGTR1 polymorphism and hsCRP levels, which appears to be independent of anthropometric and metabolic traits, is yet another indication of a direct influence of RAS on inflammation.

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