Li Wang, Shaofang Shangguan, Shaoyan Chang, Xin Yu, Zhen Wang, Xiaolin Lu, Lihua Wu, Ting Zhang
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{"title":"Determining the association between methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms and genomic DNA methylation level: A meta-analysis","authors":"Li Wang, Shaofang Shangguan, Shaoyan Chang, Xin Yu, Zhen Wang, Xiaolin Lu, Lihua Wu, Ting Zhang","doi":"10.1002/bdra.23511","DOIUrl":null,"url":null,"abstract":"<div>\n \n <section>\n \n <h3> Background</h3>\n \n <p>The methylenetetrahydrofolate reductase (<i>MTHFR</i>) polymorphism is a risk factor for neural tube defects. C677T and A1298C <i>MTHFR</i> polymorphisms produce an enzyme with reduced folate-related one carbon metabolism, and this has been associated with aberrant methylation modifications in DNA and protein.</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>A meta-analysis was conducted to assess the association between <i>MTHFR</i> C677T/A1298C genotypes and global genomic methylation.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>Eleven studies met the inclusion criteria. Of these, 10 were performed on C677T <i>MTHFR</i> genotypes and 6 were performed on A1298C <i>MTHFR</i> genotypes. Our results did not indicate any correlation between global methylation and <i>MTHFR</i> A1298C, C677T polymorphisms.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>The results of our study provide evidence to assess the global methylation modification alterations of <i>MTHFR</i> polymorphisms among individuals. However, our data did not found any conceivable proof supporting the hypothesis that common variant of <i>MTHFR</i> A1298C, C677T contributes to methylation modification. Birth Defects Research (Part A) 106:667–674, 2016. © 2016 Wiley Periodicals, Inc.</p>\n </section>\n </div>","PeriodicalId":8983,"journal":{"name":"Birth defects research. Part A, Clinical and molecular teratology","volume":"106 8","pages":"667-674"},"PeriodicalIF":0.0000,"publicationDate":"2016-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/bdra.23511","citationCount":"13","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Birth defects research. Part A, Clinical and molecular teratology","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/bdra.23511","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 13
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确定亚甲基四氢叶酸还原酶(MTHFR)基因多态性与基因组DNA甲基化水平之间的关系:一项荟萃分析
背景亚甲基四氢叶酸还原酶(MTHFR)多态性是神经管缺陷的危险因素。C677T和A1298C MTHFR多态性产生一种与叶酸相关的一碳代谢减少的酶,这与DNA和蛋白质的异常甲基化修饰有关。方法采用meta分析评估MTHFR C677T/A1298C基因型与全球基因组甲基化的关系。结果11项研究符合纳入标准。其中C677T MTHFR基因型10例,A1298C MTHFR基因型6例。我们的研究结果没有显示全局甲基化与MTHFR A1298C, C677T多态性之间的任何相关性。结论本研究结果为评估个体间MTHFR多态性的整体甲基化修饰改变提供了依据。然而,我们的数据没有发现任何可想象的证据支持MTHFR A1298C, C677T共同变异有助于甲基化修饰的假设。出生缺陷研究(分册),2016.(06):667 - 674。©2016 Wiley期刊公司
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