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Angiotensinogen-M235T as a risk factor for myocardial infarction in Asian populations: a genetic association study and a bioinformatics approach.

ABSTRACT: AIM:To investigate if there is an association between M235T polymorphism of angiotensinogen gene and myocardial infarction (MI) risk and perform a meta-analysis and an in silico approach. METHODS:This case-control study included 340 participants (155 MI patients and 185 controls) examined at Kashan University of Medical Sciences (Kashan, Iran) between 2013 and 2015. Meta-analysis included 25 studies with 6334 MI patients and 6711 controls. Bioinformatics tools were applied to evaluate the impact of M235T polymorphism on angiotensinogen function and structure. RESULTS:Genetic association study revealed a significant association between TT genotype (odds ratio [OR] 2.08, 95% confidence interval [CI] 1.08-4.00, P=0.029) and T allele (OR 1.45, 95% CI 1.06-1.99, P=0.021) and MI risk. Meta-analysis also revealed a significant association between M235T polymorphism and MI risk in allelic (OR 1.55, 95% CI 1.10-2.18, P=0.012) and recessive (OR 1.69, 95% CI 1.13-2.53, P=0.010) models within Asian population. In silico-analysis revealed that M235T fundamentally changed the function of angiotensinogen (score 32; expected accuracy 66%). CONCLUSIONS:Our study suggests that M235T polymorphism might be a helpful biomarker for screening of susceptible individuals for MI in Asian population.

SUBMITTER: Raygan F

PROVIDER: S-EPMC5048226 | biostudies-literature | 2016 Aug

REPOSITORIES: biostudies-literature

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Angiotensinogen-M235T as a risk factor for myocardial infarction in Asian populations: a genetic association study and a bioinformatics approach.

Raygan Fariba F Karimian Mohammad M Rezaeian Atefeh A Bahmani Bahareh B Behjati Mohaddeseh M

Croatian medical journal 20160801 4

<h4>Aim</h4>To investigate if there is an association between M235T polymorphism of angiotensinogen gene and myocardial infarction (MI) risk and perform a meta-analysis and an in silico approach.<h4>Methods</h4>This case-control study included 340 participants (155 MI patients and 185 controls) examined at Kashan University of Medical Sciences (Kashan, Iran) between 2013 and 2015. Meta-analysis included 25 studies with 6334 MI patients and 6711 controls. Bioinformatics tools were applied to eval ...[more]

PMID: 27586550

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Project description:MicroRNAs (miRNAs) are a class of highly conserved endogenous noncoding single-stranded small RNAs with a length of 18-22 nucleotides. They are involved in regulation at the posttranscriptional and translational levels through the degradation and translation inhibition of messenger RNA (mRNA). It is estimated that at least 60% of all mammalian genes may be regulated by miRNAs. MiRNAs can help uncover the mechanisms of diseases and provide new entry points into therapy. Accumulated evidence has revealed that miRNAs are involved in the pathological process of cardiovascular disease through specific signaling pathways. To investigate the potential miRNAs for myocardial fibrosis post myocardial infarction, rat models of acute myocardial infarction (AMI) were established by ligating the anterior descending branch of the left coronary artery, while sham-operated rats were only threaded without ligation as a control group. There were three rats in each group. Thirteen differentially expressed miRNAs between the two groups were screened and their expression levels in the model group were all higher than those in the control group. The expression of miR-199a-5p was significantly increased in the model group in qRT-PCR, which was consistent with the results of the gene chip. KEGG enrichment analysis showed that the target genes of miR-199a-5p were enriched in the insulin signaling pathway. Furthermore, dual-luciferase reporter assay indicated that miR-199a-5p could negatively regulate the expression of GSK-3β. After transfection, the expression of miR-199a-5p was increased in the miR-199a-5p mimics group. The protein expression of GSK-3β was decreased in CFs transfected with miR-199a-5p mimics. In summary, our study identified miR-199a-5p could promote the progression of myocardial fibrosis after myocardial infarction by targeting GSK-3β, which provides novel targets for diagnosis and treatment of MF. In summary, our research suggests that miR-199a-5p promotes the progression of myocardial fibrosis after myocardial infarction through the activation of the insulin-PI3K/Akt-GSK-3β signaling pathway.

Dataset Information

Angiotensinogen-M235T as a risk factor for myocardial infarction in Asian populations: a genetic association study and a bioinformatics approach.

Publications

Angiotensinogen-M235T as a risk factor for myocardial infarction in Asian populations: a genetic association study and a bioinformatics approach.

Similar Datasets

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