Identification of potential molecular mechanisms and candidate genes involved in the acute phase of myocardial infarction

Objective: This study used bioinformatics to determine genetic factors involved in progression of acute myocardial infarction [MI]

Materials and Methods: In this prospective study, gene expression profile GSE59867 was downloaded from the Gene Expression Omnibus database, which contained 46 normal samples obtained from stable coronary artery disease patients [n=46] who were without history of MI [control] and 390 samples from patients [n=111] who had evolving ST-segment elevation myocardial infarction [STEMI] as the MI group. These samples were divided into 4 groups based on time points. After identification of differentially expressed genes [DEGs], we conducted hierarchical clustering and functional enrichment analysis. Protein interaction and transcriptional regulation among DEGs were analysed

Results: We observed 8 clusters of DEGs that had a peak or a minimum at the t=1 time point according to gene expression levels. Upregulated DEGs showed significant enrichment in the biological process, single-organism cellular process, response to stimulus and stress, and osteoclast differentiation and lysosome. Downregulated DEGs enriched in the T-cell receptor signalling pathway and natural killer cell mediated cytotoxicity. We identified multiple genes, including signal transducer and activator of transcription 3 [STAT3]; LCK proto-oncogene, Src family tyrosine kinase [LCK]; and FYN proto-oncogene, Src family tyrosine kinase [FYN] from the protein-protein interaction [PPI] network and/or the transcriptional regulatory network

Conclusion: Cytokine-mediated inflammation, lysosome and osteoclast differentiation, and metabolism processes, as well as STAT3 may be involved in the acute phase of MI

Expressions of nitric oxide and plasminogen activator inhibitor type-1 in rabbit models of atherosclerosis and interference effect of atorvastatin / 吉林大学学报(医学版)

0.05).The levels of serum TC in groups A,B,and C were (23.51?10.58),(14.27?3.51)and(1.36?0.33)mmol?L-1, respectively; the levels of serum LDL in groups A,B,and C were (21.39?10.00),(14.23?4.01)and(0.72?0.35)mmol?L-1;there were significant differences between three groups (P0.05).Conclusion High-fat diet has no significant effect on the expressions of NO and PAI-1 in atherosclerosis rabbits .Atorvastatin can increase the expression of NO and decrease the expression of PAI-1,and can inhibit the progression of atherosclerosis.