Complex analysis of association of inflammation gene polymorphisms with myocardial infarction

Судомоина, М. А.; Сухинина, Т. С.; Barsova, R. M.; Favorov, Alexander V.; Sakhnovich, R. M.; Титов, Б. В.; Матвеева, Н. А.; Rybalkin, I. N.; Власик, Т. Н.; Ochs, Michael F.; Ruda, Mikhail; Фаворова, О. О.

doi:10.1134/s0026893310030088

Cited by 15 publications

(13 citation statements)

References 29 publications

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“…Associations of certain alleles and geno types were not observed either with the predisposition to cardiac infarction or with an unfavorable outcome upon ACS. At the same time, the frequencies of geno types of the -174G>C polymorphic region obtained in the present work for the control subjects corre sponded to the frequencies of genotypes in patients with ACS [32], in patients with cardiac infarction, and in the control subjects (our unpublished data for the sampling investigated in [31]). At the same time, in both cases [31,32], combinations of alleles and geno types of IL6 and other inflammation genes were revealed which are associated with the disease.…”

Section: Resultsmentioning

confidence: 54%

“…At the same time, the frequencies of geno types of the -174G>C polymorphic region obtained in the present work for the control subjects corre sponded to the frequencies of genotypes in patients with ACS [32], in patients with cardiac infarction, and in the control subjects (our unpublished data for the sampling investigated in [31]). At the same time, in both cases [31,32], combinations of alleles and geno types of IL6 and other inflammation genes were revealed which are associated with the disease. We dis covered a protective effect of carriage of the IL6*-174C allele in combination with CCR5*d (rs333) and LTA*252G (rs909253) in the development of cardiac inf arction [31]; the association of an unfavorable outcome with combined carriage of the -174G/G genotype of IL6 and 1082G/A and 1082A/A genotypes of IL10 was revealed in patients with ACS [32].…”

Section: Resultsmentioning

confidence: 54%

“…At the same time, in both cases [31,32], combinations of alleles and geno types of IL6 and other inflammation genes were revealed which are associated with the disease. We dis covered a protective effect of carriage of the IL6*-174C allele in combination with CCR5*d (rs333) and LTA*252G (rs909253) in the development of cardiac inf arction [31]; the association of an unfavorable outcome with combined carriage of the -174G/G genotype of IL6 and 1082G/A and 1082A/A genotypes of IL10 was revealed in patients with ACS [32]. Comparison of these data with our results indicates a unidirectional influence of the polymorphic variants of SNP-174G>C of IL6 on the development of cardiovascular diseases: G is the risk allele and C is the protective allele exhibited more clearly in IS than in ischemic heart disease.…”

Section: Resultsmentioning

confidence: 94%

“…The association of -174G>C polymorphism of IL6 with the development of cardiovascular diseases in ethnic Russians was analyzed earlier upon cardiac inf arction [31] and acute coronary syndrome (ACS) [32], but not IS. Associations of certain alleles and geno types were not observed either with the predisposition to cardiac infarction or with an unfavorable outcome upon ACS.…”

Section: Resultsmentioning

confidence: 99%

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Polymorphic variants of the genes encoding intrleukin-6 and fibrinogen: Risk for ischemic stroke and fibrinogen levels

et al. 2012

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The occurrence of alleles and genotypes of polymorphic region -174G>C of the gene IL6 (rs1800795) in patients of Russian ethnicity with ischemic stroke (200 cases) and in the control of the same ethnicity similar in sex and age (140 control subjects) has been analyzed. Reliable differences were revealed in the carriage frequency of allele IL6*-174G in homozygous and heterozygous form (p = 0.0029, OR = 2.9, 95% CI: 1.4-5.8), which can be considered a risk factor for the development of ischemic stroke, and in the carriage frequencies of protective genotype IL6*-174C/C (p = 0.0029, OR = 0.35, 95% CI: 0.17-0.69), respectively. After the patients and the control subjects were divided by gender character, similar differences were observed only between women with ischemic stroke and those from the control group, and after division by age, they were only revealed in groups with members older than 60 years. Complex analysis of the associ ation of ischemic stroke with the carriage of alleles and genotypes of IL6 SNP-174G>C in combination with SNP 4266A>G (Thr312Ala) of the gene FGA (rs6050) and -249C>T of the gene FGB (rs1800788) revealed protective combinations of IL6*-174C/C + FGA*4266A and IL6*-174C/C + FGB*-249C, which are slightly more reliably associated with ischemic stroke than the one protective genotype IL6* -174C/C and have nearly the same OR value . At the same time, combinations of alternative allele IL6*-174G and the same alleles FGA*4266A or FGB*-249C were revealed that are characterized by a decrease in both the significance level and the OR value as compared with the carriage of one risk allele IL6*-174G. When there is a combined carriage of the allele IL6*-174G with the genotypes FGA*4266A/A, FGB*-249C/C or with combinations of these alleles/genotypes, the neutralizing effect is enhanced. In other words, we observed the association of IL6, FGA and FGB allele combinations with ischemic stroke in which IL6 plays the key role and FGA and FGB have a modulating function. In analyzing the association of the alleles/genotypes of three polymorphic regions with the fibrinogen level in plasma, no reliable difference was revealed.

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Section: Resultsmentioning

confidence: 54%

Section: Resultsmentioning

confidence: 54%

Section: Resultsmentioning

confidence: 94%

Section: Resultsmentioning

confidence: 99%

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Polymorphic variants of the genes encoding intrleukin-6 and fibrinogen: Risk for ischemic stroke and fibrinogen levels

et al. 2012

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“…This may be due to the fact that sample sizes of many studies included in our meta-analysis were relatively small (Rich, 2006); the number of eligible studies included in total was also not enough. In addition, 3 potential studies in Russia were not included due to publication language and difficulties in accessing Russian databases (Shevchenko et al, 2010;Sudomoina et al, 2010;Konenkov et al, 2012). It is known that there are several polymorphisms associated with MI risk, but the gene-gene interactions were not addressed in our current meta-analysis due to insufficient data.…”

Section: Discussionmentioning

confidence: 99%

Association between TNF-α rs1800629 polymorphism and the risk of myocardial infarction: A meta-analysis

et al. 2016

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ABSTRACT. The tumor necrosis factor-alpha (TNF-α) G-308A polymorphism has been suggested to be a susceptibility factor for myocardial infarction (MI). However, differing results from various studies have led to controversial conclusions. Hence, we performed a meta-analysis to evaluate the association between TNF-α G-308A polymorphism and MI. Reported studies published before March 30, 2015 were included and analyzed from the PubMed and Embase databases. Study selection and data extraction were carried out independently by two authors. The odds ratios (ORs) and 95% confidence intervals (CIs) were used to evaluate the association between the selected variables using the Comprehensive Meta-Analysis v2.2 software. In total, 12 publications with 13 case-control studies consisting of 6037 cases and 7262 controls However, when subgroup analysis was performed according to the stages of MI, results indicated that there was a significant association between TNF-α G-308A polymorphism and the risk of acute MI. Other subgroup analyses revealed no significant associations. Current evidence suggests that TNF-α G-308A polymorphism may be associated with increased risk for acute MI.

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Identification of NF‐κB inhibitors in Qishenyiqi dropping pills for myocardial infarction treatment based on bioactivity‐integrated UPLC‐Q/TOF MS

Han

Zhou

Xing

et al. 2015

Biomedical Chromatography

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Qishenyiqi dropping pills (QSYQ) are a type of standardized cardiovascular multiherb medicine for the treatment of myocardial infarction (MI). Knowledge concerning the systemic identification of nuclear factor-kappa B (NF-κB) inhibitors of QSYQ is generally lacking. Therefore, it is necessary to establish an effective method to screen the bioactive components of NF-κB inhibition. In the present study, a rat model of coronary artery ligation was used to assess the cardioprotective effects of QSYQ. The electrocardiograms, histopathology of heart tissues and serum biochemical indicators, such as brain natriuretic peptide, cardiac troponin I and inflammatory cytokines, were measured. Subsequently, ultra-performance liquid chromatography quadrupole/time-of-flight mass spectrometry (UPLC-Q/TOF MS) combined with the NF-κB luciferase reporter assay system was applied to screen the potential anti-inflammatory compounds in QSYQ. The results revealed that the administration of QSYQ could improve heart function, ameliorate neutrophil infiltration and diminish the levels of inflammatory cytokines in MI rats. Furthermore, 22 compounds were determined to be potential NF-κB inhibitors. In conclusion, NF-κB inactivation and cytokine suppression might be the main mechanisms of QSYQ for MI treatment. The method of UPLC-Q/TOF MS combined with a bioactive human cell functional evaluation system was proved to be a simple and effective strategy for screening bioactive compounds in traditional Chinese medicine prescriptions.

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Complex analysis of association of inflammation gene polymorphisms with myocardial infarction

Cited by 15 publications

References 29 publications

Polymorphic variants of the genes encoding intrleukin-6 and fibrinogen: Risk for ischemic stroke and fibrinogen levels

Polymorphic variants of the genes encoding intrleukin-6 and fibrinogen: Risk for ischemic stroke and fibrinogen levels

Association between TNF-α rs1800629 polymorphism and the risk of myocardial infarction: A meta-analysis

Identification of NF‐κB inhibitors in Qishenyiqi dropping pills for myocardial infarction treatment based on bioactivity‐integrated UPLC‐Q/TOF MS

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