title: Altered gene expression pattern in peripheral blood mononuclear cells in patients with acute myocardial infarction.
abstract: BACKGROUND
  Despite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients.
  
  
  RESULTS
  Twenty-eight patients with ST-segment elevation myocardial infarction (STEMI) were included. The blood was collected on the 1(st) day of myocardial infarction, after 4-6 days, and after 6 months. Control group comprised 14 patients with stable coronary artery disease, without history of myocardial infarction. Gene expression analysis was performed with Affymetrix Human Gene 1.0 ST microarrays and GCS3000 TG system. Lists of genes showing altered expression levels (fold change >1.5, p<0.05) were submitted to Ingenuity Pathway Analysis. Gene lists from each group were examined for canonical pathways and molecular and cellular functions. Comparing acute phase of MI with the same patients after 6 months (stable phase) and with control group we found 24 genes with changed expression. In canonical analysis three pathways were highlighted: signaling of PPAR (peroxisome proliferator-activated receptor), IL-10 and IL-6 (interleukin 10 and 6).
  
  
  CONCLUSIONS
  In the acute phase of STEMI, dozens of genes from several pathways linked with lipid/glucose metabolism, platelet function and atherosclerotic plaque stability show altered expression. Up-regulation of SOCS3 and FAM20 genes in the first days of myocardial infarction is observed in the vast majority of patients.
authors.affiliation: First Chair and Department of Cardiology, Medical University of Warsaw, Warsaw, Poland. kiliszek@mp.pl
authors.forename: Marek
authors.initials: M
authors.lastname: Kiliszek
authors.forename: Beata
authors.initials: B
authors.lastname: Burzynska
authors.forename: Marcin
authors.initials: M
authors.lastname: Michalak
authors.forename: Monika
authors.initials: M
authors.lastname: Gora
authors.forename: Aleksandra
authors.initials: A
authors.lastname: Winkler
authors.forename: Agata
authors.initials: A
authors.lastname: Maciejak
authors.forename: Agata
authors.initials: A
authors.lastname: Leszczynska
authors.forename: Ewa
authors.initials: E
authors.lastname: Gajda
authors.forename: Janusz
authors.initials: J
authors.lastname: Kochanowski
authors.forename: Grzegorz
authors.initials: G
authors.lastname: Opolski
mesh_terms: D000368:Aged; D003324:Coronary Artery Disease / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D003746:Dental Enamel Proteins / Q000235:genetics* / Q000378:metabolism; D005260:Female; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D020411:Oligonucleotide Array Sequence Analysis; D047492:Peroxisome Proliferator-Activated Receptors / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000235:genetics* / Q000378:metabolism
chemical_list: D003746:Dental Enamel Proteins; C571509:FAM20A protein, human; C508609:IL10 protein, human; C508600:IL6 protein, human; D015850:Interleukin-6; D047492:Peroxisome Proliferator-Activated Receptors; C106644:SOCS3 protein, human; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D016753:Interleukin-10