Analysis of the XRCCI gene as a modifier of the cerebral response in ischemic stroke
Analysis of the XRCCI gene as a modifier of the cerebral response in ischemic stroke
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DOI：
10.1186/1471-2350-7-78
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发表时间：
2006-11-06
影响因子：
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通讯作者：
Grewal, Raji P.
中科院分区：
文献类型：
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作者：
Dutra, Ana V. C.;Lin, Hsiu-Fen;Grewal, Raji P.
背景资料：虽然有研究的遗传风险因素在发展中的中风，有很少的调查基因的作用，在脑缺血反应。大脑对缺血的一系列反应最终影响中风的体积，通常与残疾相关。我们推测，这些反应中涉及的蛋白质编码基因的多态性可以作为这种反应的修饰剂，并影响每搏输出量。参与脑缺血反应的途径之一涉及可引起核酸氧化损伤的活性氧。DNA修复机制是到位的，以防止这种损害，并意味着DNA修复基因在脑缺血的反应中的作用，是潜在的候选基因进一步investigation.Methods：我们研究了两个常见的多态性DNA修复基因，XRCC 1，C26304 T和G28152 A，在134个特点的非腔隙性缺血性中风患者。我们还对113名对照患者进行了病例对照关联研究，以评估这些变异是否代表缺血性卒中发生的危险因素。结果：与病因无关，C26304 T多态性的“T”等位基因与较大的卒中量显著相关（T检验分析，p < 0.044;多变量回归分析，β = 0.23，p < 0.008）。在病例对照关联研究中，我们发现，这些多态性都没有代表一个危险因素的发展stroke.Conclusion：我们的研究表明，一个主要的基因效应的“T”等位基因的C26304 T多态性调制脑缺血反应在非腔隙性缺血性中风。
Background: Although there have been studies of the genetic risk factors in the development of stroke, there have been few investigations of role of genes in the cerebral response to ischemia. The brain responds to ischemia in a series of reactions that ultimately influence the volume of a stroke that, in general, correlates with disability. We hypothesize that polymorphisms in genes encoding proteins involved in these reactions could act as modifiers of this response and impact stroke volume. One of the pathways participating in the cerebral ischemic response involves reactive oxygen species which can cause oxidative damage to nucleic acids. DNA repair mechanisms are in place to protect against such damage and imply a role for DNA repair genes in the response of the brain to ischemia and are potential candidate genes for further investigation.Methods: We studied two common polymorphisms in the DNA repair gene, XRCC1, C26304T and G28152A, in 134 well characterized patients with non lacunar ischemic strokes. We also performed a case control association study with 113 control patients to assess whether these variants represent risk factors in the development of ischemic stroke.Results: Independent of etiology, the "T" allele of the C26304T polymorphism is significantly associated with larger stroke volumes (T-test analysis, p < 0.044; multivariate regression analysis, beta = 0.23, p < 0.008). In the case control association study, we found that neither of these polymorphisms represented a risk factor for the development of stroke.Conclusion: Our study suggests a major gene effect of the "T" allele of the C26304T polymorphism modulating the cerebral response to ischemia in non lacunar ischemic stroke.