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Interplay Between miR-155, AT1R A1166C Polymorphism, and AT1R Expression in Young Untreated Hypertensives

Interplay Between miR-155, AT1R A1166C Polymorphism, and AT1R Expression in Young Untreated... BackgroundA silent polymorphism (+1166 A/C single-nucleotide polymorphism) localized in the 3′-UTR (untranslated region) of the human angiotensin II type-1 receptor (AT1R) has been associated with hypertension and cardiovascular complications. The +1166 A/C is recognized by a specific microRNA-155 (miR-155), which is basepairing complementary with the +1166 A-allele but not with the mutant +1166 C allele. Aim of our study was to investigate the interplay between miR-155 and AT1R protein expression.MethodsSixty-four subjects were selected for the +1166 A/C from the cohort of hypertensives (n = 573) of the Hypertension and Ambulatory Recording Venetia Study (HARVEST): 25 were homozygous for the 1166 A allele, 20 heterozygous, and 19 homozygous for the 1166 C allele.ResultsmiR-155 expression was significantly decreased in subjects with CC genotype in comparison to AA and AC genotype. AT1R protein expression was significantly increased in the CC group in comparison to AA and AC (P < 0.01) although AT1R mRNA expression was not significantly different in the three groups. AT1R protein expression was positively correlated with systolic and diastolic blood pressure and negatively correlated with miR-155 expression level. Plasma transforming growth factor-β1 (TGF-β1) may have a modulator role in the interplay between miR-155 and AT1R protein expression as it was correlated negatively with miR-155 expression and positively with AT1R protein expression in subjects with CC genotype.ConclusionThe interplay between miR-155 expression, +1166C polymorphism,and AT1R protein expression may have a role in the regulation of blood pressure. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Journal of Hypertension Oxford University Press

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References (31)

Publisher
Oxford University Press
Copyright
© 2011 by the American Journal of Hypertension, Ltd.
Subject
Renin-Angiotensin-Aldosterone System
ISSN
0895-7061
eISSN
1941-7225
DOI
10.1038/ajh.2010.211
pmid
20966899
Publisher site
See Article on Publisher Site

Abstract

BackgroundA silent polymorphism (+1166 A/C single-nucleotide polymorphism) localized in the 3′-UTR (untranslated region) of the human angiotensin II type-1 receptor (AT1R) has been associated with hypertension and cardiovascular complications. The +1166 A/C is recognized by a specific microRNA-155 (miR-155), which is basepairing complementary with the +1166 A-allele but not with the mutant +1166 C allele. Aim of our study was to investigate the interplay between miR-155 and AT1R protein expression.MethodsSixty-four subjects were selected for the +1166 A/C from the cohort of hypertensives (n = 573) of the Hypertension and Ambulatory Recording Venetia Study (HARVEST): 25 were homozygous for the 1166 A allele, 20 heterozygous, and 19 homozygous for the 1166 C allele.ResultsmiR-155 expression was significantly decreased in subjects with CC genotype in comparison to AA and AC genotype. AT1R protein expression was significantly increased in the CC group in comparison to AA and AC (P < 0.01) although AT1R mRNA expression was not significantly different in the three groups. AT1R protein expression was positively correlated with systolic and diastolic blood pressure and negatively correlated with miR-155 expression level. Plasma transforming growth factor-β1 (TGF-β1) may have a modulator role in the interplay between miR-155 and AT1R protein expression as it was correlated negatively with miR-155 expression and positively with AT1R protein expression in subjects with CC genotype.ConclusionThe interplay between miR-155 expression, +1166C polymorphism,and AT1R protein expression may have a role in the regulation of blood pressure.

Journal

American Journal of HypertensionOxford University Press

Published: Feb 1, 2011

Keywords: angiotensin II angiotensin receptor type 1 arterial hypertension blood pressure gene expression hypertension microRNA miR-155 protein expression

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