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首页> 外文期刊>Genomics >Left ventricular global transcriptional profiling in human end-stage dilated cardiomyopathy.
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Left ventricular global transcriptional profiling in human end-stage dilated cardiomyopathy.

机译：人类终末期扩张型心肌病的左心室整体转录谱。

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摘要

We employed ABI high-density oligonucleotide microarrays containing 31,700 sixty-mer probes (representing 27,868 annotated human genes) to determine differential gene expression in idiopathic dilated cardiomyopathy (DCM). We identified 626 up-regulated and 636 down-regulated genes in DCM compared to controls. Most significant changes occurred in the tricarboxylic acid cycle, angiogenesis, and apoptotic signaling pathways, among which 32 apoptosis- and 13 MAPK activity-related genes were altered. Inorganic cation transporter, catalytic activities, energy metabolism and electron transport-related processes were among the most critically influenced pathways. Among the up-regulated genes were HTRA1 (6.9-fold), PDCD8(AIFM1) (5.2) and PRDX2 (4.4) and the down-regulated genes were NR4A2 (4.8), MX1 (4.3), LGALS9 (4), IFNA13 (4), UNC5D (3.6) and HDAC2 (3) (p<0.05), all of which have no clearly defined cardiac-related function yet. Gene ontology and enrichment analysis also revealed significant alterations in mitochondrial oxidative phosphorylation, metabolism and Alzheimer's disease pathways. Concordance was also confirmed for a significant number of genes and pathways in an independent validation microarray dataset. Furthermore, verification by real-time RT-PCR showed a high degree of consistency with the microarray results. Our data demonstrate an association of DCM with alterations in various cellular events and multiple yet undeciphered genes that may contribute to heart muscle disease pathways.
机译：我们采用包含31,700个60-mer探针（代表27,868个带注释的人类基因）的ABI高密度寡核苷酸微阵列来确定特发性扩张型心肌病（DCM）中的差异基因表达。与对照相比，我们在DCM中鉴定了626个上调基因和636个下调基因。最重要的变化发生在三羧酸循环，血管生成和凋亡信号通路中，其中32个凋亡相关基因和13个MAPK活性相关基因被改变。无机阳离子转运蛋白，催化活性，能量代谢和电子输送相关过程是受影响最严重的途径。上调的基因是HTRA1（6.9倍），PDCD8（AIFM1）（5.2）和PRDX2（4.4），而下调的基因是NR4A2（4.8），MX1（4.3），LGALS9（4），IFNA13（ 4），UNC5D（3.6）和HDAC2（3）（p <0.05），所有这些都没有明确定义的心脏相关功能。基因本体论和富集分析还揭示了线粒体氧化磷酸化，代谢和阿尔茨海默氏病途径的显着改变。在独立的验证微阵列数据集中，也证实了大量基因和途径的一致性。此外，通过实时RT-PCR的验证显示与微阵列结果高度一致。我们的数据证明了DCM与各种细胞事件以及可能有助于心肌疾病途径的多个尚未破译的基因发生改变的关联。

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