Abstract

The aim of this study was to investigate the relationship between gene Period3 (Per3) variable number tandem repeat (VNTR) polymorphism and chronic heart failure (CHF). The study subjects (372 patients of Caucasian origin with CHF and 332 healthy controls) were genotyped for Per3 VNTR polymorphism using an allele-specific PCR. No significant differences in genotype or Per3 VNTR allele frequencies were found between CHF cases and controls (Pg=0.30, Pa=0.52). No significant differences were uncovered either between CHF cases according to etiology (DCMP vs. IHD; Pg=0.87, Pa=0.91). In the multivariate regression modeling, no predictive function of VNTR Per3 polymorphism on ejection fraction or NYHA class, hyperlipidaemia or type II diabetes risk was found. Per3 VNTR polymorphism is not a major risk factor for chronic heart failure or a factor modulating the severity of the CHF in this population.

Highlights

  • Many physiological processes in the organism exhibit daily rhythmicity, which is generated by an internal “clock” setting about 24-h periodic expression of clock genes and their products

  • Per[3] VNTR polymorphism is not a major risk factor for chronic heart failure or a factor modulating the severity of the CHF in this population

  • Circadian clock regulation has been identified in almost every human cell to date, suggesting a wide-ranging role of a light-dark dependent modulation on physiological and pathophysiological events

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Summary

Introduction

Many physiological processes in the organism exhibit daily rhythmicity, which is generated by an internal “clock” setting about 24-h periodic expression of clock genes and their products. Such reliable biological oscillators allow almost every cell to predict environmental changes and accurately react to them. According to the basic model of the function of “core clock proteins”, the principal components of the positive loop BMAL1 and CLOCK periodically activate the transcription of Per and Cry genes. The Per and Cry complexes, after reaching threshold concentration, interact with BMAL1 and CLOCK and repress their transcription generating nearly antiphasic expression[8,9]

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