HDAC9 Variant Rs2107595 Modifies Susceptibility to Coronary Artery Disease and the Severity of Coronary Atherosclerosis in a Chinese Han PopulationReport as inadecuate




HDAC9 Variant Rs2107595 Modifies Susceptibility to Coronary Artery Disease and the Severity of Coronary Atherosclerosis in a Chinese Han Population - Download this document for free, or read online. Document in PDF available to download.

A previous genome-wide association study showed that a single nucleotide polymorphism SNP rs2107595 in histone deacetylase 9 HDAC9 gene was associated with large artery stroke LAS in Caucasians. Based on the similar atherosclerotic pathogenesis between LAS and coronary artery disease CAD, we aimed to evaluate the associations of SNP rs2107595 with CAD risk and the severity of coronary atherosclerosis in a Chinese Han population, and explore the potential gene-environment interactions among SNP rs2107595 and conventional CAD risk factors. In a two-stage case-control study with a total of 2317 CAD patients and 2404 controls, the AG + AA genotypes of SNP rs2107595 were significantly associated with increased CAD risk Adjusted odds ratio OR = 1.23, Padj = 0.001 and higher modified Gensini scores Adjusted OR = 1.38, Padj < 0.001. These associations remained significant in subtype analyses for unstable angina pectoris UAP, non-ST-segment elevation myocardial infarction NSTEMI and ST-segment elevation myocardial infarction STEMI. Subgroup and multifactor dimensionality reduction analyses MDR further found the gene-environment interactions among SNP rs2107595, body mass index, type 2 diabetes and hyperlipidemia in CAD risk and the severity of coronary atherosclerosis. Moreover, patients with CAD had higher levels of HDAC9 mRNA expression and plasma HDAC9 than controls. Subsequent genotype-phenotype analyses observed the significant correlations of SNP rs2107595 with HDAC9 mRNA expression and plasma HDAC9 levels in controls and patients with NSTEMI and STEMI. Taken together, our data suggest that SNP rs2107595 may contribute to coronary atherosclerosis and CAD risk through a possible mechanism of regulating HDAC9 expression and gene-environment interactions.



Author: Xue-bin Wang , Ya-di Han , Shrestha Sabina, Ning-hua Cui, Shuai Zhang, Ze-jin Liu, Cong Li, Fang Zheng

Source: http://plos.srce.hr/



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