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Association Between the Gene Polymorphisms of HDAC9 and the Risk of Atherosclerosis and Ischemic Stroke

  • Original Article
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Pathology & Oncology Research

Abstract

Genome-wide association studies have demonstrated various polymorphisms of histone deacetylase 9 (HDAC9) gene was strong risk locus for large-vessel stroke, but the results were controversial. This study aims to replicate the association between the previous detected SNPs of HDAC9 and the susceptibility of ischemic stroke. The study population consisted of 262 consecutive patients diagnosed with ischemic stroke and 300 age and gender matched unrelated controls between October 2012 and October 2014. Rs11984041, rs2389995, and rs2240419 of HDAC9 were genotyped and compared between the cases and controls. The SNP rs11984041 of HDAC9 was found nonpolymorphic in the population involved. The G allele of rs2389995 was found significantly associated with decreased risk of ischemic stroke, no matter with the codominant (AG v.s AA, 0.53 (0.36–0.77), P < 0.001; GG v.s AA, 0.63 (0.27–1.43), P < 0.001), dominant (AG + GG v.s AA, 0.54 (0.38–0.78), P < 0.001), or the recessive model (GG vs AA + AG, 0.75 (0.33–1.71), P < 0.001). On the other hand, The T allele of rs2240419 was found significantly associated with increased risk of ischemic stroke, no matter with the codominant (CT v.s CC, 1.75 (1.22–2.51), P < 0.001; TT v.s CC, 2.67 (1.55–4.61), P < 0.001), dominant (CT + TT v.s CC, 1.93 (1.38–2.71), P < 0.001), or the recessive model (TT vs CC + CT, 2.07 (1.23–3.47), P < 0.001). No linkage disequilibrium was found between rs2389995 and rs2240419 of HDAC9. In conclusion, the present study demonstrated the SNP rs11984041 of HDAC9 was nonpolymorphic in Chinese Han population. The minor G allele of rs2389995 significantly decreased and the minor T allele of rs2240419 significantly increased the risk of ischemic stroke.

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qingxu, G., Yan, Z., Jiannan, X. et al. Association Between the Gene Polymorphisms of HDAC9 and the Risk of Atherosclerosis and Ischemic Stroke. Pathol. Oncol. Res. 22, 103–107 (2016). https://doi.org/10.1007/s12253-015-9978-8

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  • DOI: https://doi.org/10.1007/s12253-015-9978-8

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