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目的本研究旨在探究差异表达基因(Differentially expressed genes,DEG),然后鉴别出急性心肌梗死(Acute myocardial infarction,AMI)关键基因,由此筛查出可用于这种研究早期诊断的心脏疾病潜在生物标记物。方法 AMI患者(GSE19339)的基因表达数据下载自基因表达汇编数据库。采用affy程序包预处理后,在samar程序包内通过微阵列显著性分析(Significance analysis of mycroarray,SAM)算法筛选DEG。然后使用DAVID(注释可视化和整合发现数据库软件,database for annotation visualization and integrated discovery software)在线工具进行DEG功能和通路富集分析。进而采用GENET-IC_ASSOCIATION_DB_DISEASE分析和blastp比对算法筛选出AMI的相关基因。最后,将这些新基因用于转录因子和蛋白-蛋白相互作用网络分析。结果在AMI患者与正常对照样本间共筛选出633个DEG,包括378个上调DEG和255个下调DEG。在AMI中发现了一种显著差异表达的新基因LCK(淋巴细胞特异性蛋白酪氨酸激酶,lymphocytespecific protein tyrosine kinase)。进一步分析显示LCK参与CXCL12(趋化因子(C-X-C基序)配体12,chemokine(C-X-Cmotif)ligand12)的表达调节,而LCK的表达则由不同的转录因子进行调节。结论这项研究中,我们对AMI的发病机制提出了新见解,并提出LCK是这种严重心脏疾病的一个引人注目的候选标记物。
Objective This study aimed to explore differentially expressed genes (DEG) and then identify the key genes of acute myocardial infarction (AMI), thus screening potential biomarkers of heart disease that can be used in the early diagnosis of such studies Mark. Methods Gene expression data for AMI patients (GSE19339) were downloaded from the Gene Expression Assembler database. After affy package preprocessing, DEG was screened by the significance analysis of mycroarray (SAM) algorithm in the samar package. Then use the online tool DAVID (annotation visualization and integrated discovery software) to perform DEG function and pathway enrichment analysis. Then the gene of AMI was screened by GENET-IC_ASSOCIATION_DB_DISEASE analysis and blastp alignment algorithm. Finally, these new genes are used in transcription factor and protein-protein interaction network analysis. Results A total of 633 DEG were screened between AMI patients and normal control samples, including 378 up-regulated DEGs and 255 down-regulated DEGs. A novel, significantly differentially expressed, LCK (lymphocyte-specific protein tyrosine kinase) was found in AMI. Further analysis showed that LCK is involved in the regulation of CXCL12 (chemokine (C-X-C motif) ligand 12, chemokine (C-X-Cmotif) ligand12), whereas LCK expression is regulated by different transcription factors. Conclusions In this study, we present new insights into the pathogenesis of AMI and propose LCK as a compelling candidate marker for this serious heart disease.