Association of il-1β(-511 c / t) and il-1β (-31 t / c) gene polymorphism with endoplasmic reticulum stress marker levels in acute decompensated heart failure with low ejection fraction

Abstract

Inflammatory processes play an important role in the pathogenesis of heart failure. The accumulation of unfolded proteins in the endoplasmic reticulum lumen and the unfolded protein response signal path is activated. The IL-1? gene is located in the Chromosome 2.q14 region. -31 and -511 single nucleotide polymorphisms (SNPs) were detected in the IL-1?promoter region. These two SNPs affect IL-1expression. This study aims to investigate the presence of IL-1?(-511 C / T) and IL-1? (-31 T / C) gene polymorphisms and the relationship between ER stress markers and inflammatory markers. Patients who applied to the department of emergency medicine with the findings of acute decompensated heart failure. Polymorphic sites of theIL-1? gene were determined by DNA sequencing. In all study, individuals with IL-1?(-31 T / C) T allele have higher serum PERK, GRP-78, CHOP and CRP levels median values than individuals with IL-1?(-31 T/C) C allele (p = 0.0001, p = 0.002, p = 0.002 and p =0.011, respectively). Serum ERK and GRP-78 values in HF group were higher in individuals with IL-1?(-31 T / C) T allele compared to individuals with C allele (p = 0.0001 and p = 0.006). There was a statistically significant difference in serum CHOP levels in the control group with the IL-1? (-511 C / T) T allele and the individuals with the C allele in the HF group (p = 0.002). In conclusion, we consider that the inflammatory response caused by IL-1? (-31 T / C) gene polymorphism increased and the ER stress response increased, inflammatory pathway and ER stress of having IL-1?(-31 T / C) T / T genotype or T allele.