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目的我们旨在探索心肌梗死(MI)后梗死面积进展和扩大相关机制。方法将包含经历MI或模拟手术的雄性Wistar大鼠左心室肌的23个基因转录芯片的GSE47495微阵列数据从基因表达数据库下载。利用单因素方差分析确定差异表达基因(DEGs)。对DEG进行时间序列表达数据聚类算法和功能富集分析。利用STRING和Cytoscape分别进行蛋白质相互作用(PPI)网络的构建和可视化。对涉及PPI网络重要模块的DEG进行Intro Pro域分析。结果共确定1070个DEG,其中383个DEG(表达谱0中)随梗死面积增加而下调,499个DEG(表达谱4中)随梗死面积扩大而上调。表达谱0(0、-1、-2和-3)和表达谱4(0、1、2和3)中的DEG分别与脂肪酸氧化(如ACADM,ACOX1和EHHADH)和细胞外基质(如TGFB,COL1A1和COL3A1)相关。表达谱0和4中的DEG被划归到PPI网络的5个重要模块,模块1和模块2分别有细胞长链脂酰辅酶A脱氢酶/氧化酶(如ACADM、ACOX1和EHHADH)和原纤维胶原蛋白(如TGFB1、COL1A1和COL3A1)intro Pro域。结论代偿性MI向心力衰竭的转变可能与脂肪酸氧化失活和细胞外基质激活有关。
Objective We aimed to explore the infarction area after myocardial infarction (MI) progress and expansion of the relevant mechanisms. Methods GSE47495 microarray data from 23 gene transcripts of the left ventricular muscle of male Wistar rats undergoing MI or mock surgery were downloaded from the gene expression database. Differential expression genes (DEGs) were determined using one-way analysis of variance. Time series of DEG data clustering algorithm and function enrichment analysis. Construction and visualization of protein-protein interaction (PPI) networks using STRING and Cytoscape respectively. Intro Pro domain analysis of DEGs involving important PPI network modules. RESULTS: A total of 1070 DEGs were identified, of which 383 DEG (expression profile 0) were down-regulated with increasing infarct size and 499 DEG (expression profile 4) were up-regulated with infarct size expansion. DEG in expression profiles 0 (0, -1, -2 and -3) and expression profiles 4 (0, 1, 2 and 3) were associated with fatty acid oxidation such as ACADM, ACOX1 and EHHADH and extracellular matrix such as TGFB , COL1A1 and COL3A1). DEG in expression profiles 0 and 4 were assigned to five important modules of the PPI network. Modules 1 and 2 contained the long chain fatty acyl-CoA dehydrogenase / oxidase (eg, ACADM, ACOX1 and EHHADH) and the original Fibro-collagen (eg TGFB1, COL1A1 and COL3A1) intro Pro domains. Conclusion The transition from compensatory MI to heart failure may be related to the oxidative inactivation of fatty acids and the activation of extracellular matrix.