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Oligonucleotide microarray analysis of genes regulating apoptosis in chronically ischemic and postinfarction myocardium.

机译:少核苷酸微阵列分析慢性缺血性心肌病毒中凋亡细胞凋亡的基因分析。

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The pathology of cardiomyocyte death during and after myocardial infarction involves both necrosis and apoptosis. Although both mechanisms lead to cell death, participation of apoptosis in this process carries the potential of developing therapies influencing at least part of the population of dying cells. Therefore the aim of this study was to determine (using oligonucleotide microarrays) expression profiles of apoptosis-regulating genes in postinfarction myocardium, comparing chronically ischemic and healthy heart muscle. Tissue samples were obtained during elective surgery from the right cardiac auricles of three patients. The expression of 141 genes involved in fibrosis was assessed using the Affymetrix HG_U133A microarray. The patients' transcriptomes were compared using hierarchical clusterization. Differentiating genes were determined using regression analysis and Bland-Altman graph analysis. Hierarchical clusterization demonstrated that the profile of gene expression in postinfarction myocardium was different from that in the remaining specimens. Further statistical analysis showed two important differentiating genes: FOXO3A (underexpressed in post-MI sample) and CFLAR (overexpressed in post-MI sample). The expression of apoptosis-regulating genes is significantly different in post-MI myocardium from chronically ischemic and a nonischemic myocardium. Our results suggest that CFLAR is important in the induction of apoptosis in postinfarction cardiac tissue.
机译:心肌梗死期间和后心肌细胞死亡的病理涉及坏死和细胞凋亡。虽然这两种机制导致细胞死亡,但该过程中凋亡的参与携带潜在的疗法,这些疗法产生影响至少部分染色细胞群的疗法。因此,本研究的目的是在PostIncritict心肌中确定(使用寡核苷酸微阵列)表达调节基因的表达谱,比较慢性缺血和健康的心肌。在来自三名患者的右心耳廓的选修手术期间获得组织样品。使用Affymetrix HG_U133A微阵列评估参与纤维化的141个基因的表达。使用分层聚合物化进行比较患者的转录om。使用回归分析和Bland-Altman图分析测定差异基因。分层集群化表明,Postinfarctition Mocardium中基因表达的简谱与剩余标本中的基因表达不同。进一步的统计学分析显示出两个重要的分化基因:FOXO3A(在MI后样品中的缺陷率)和CFLAR(在MI后的过表达样品中)。从慢性缺血和嗜血性心肌中,MI心肌的表达明显不同。我们的研究结果表明,CFLAR在诱导晚期心脏组织中凋亡中是重要的。

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