title: Transcriptional activity of genes encoding interferon gamma (IFNgamma) and its receptor assessed in peripheral blood mononuclear cells in patients with cardiac syndrome X.
abstract: BACKGROUND
  Cardiac syndrome X is typically characterized by effort induced anginal pain with ST segment depression suggestive of myocardial ischemia and normal coronary arteries at angiography. The possible mechanism that may participate in the pathology of CSX is a microvascular dysfunction related to inflammatory process affecting endothelium. Interferon gamma (IFN-gamma) is an important cytokine in inflammatory reaction. It acts through its specific receptor composed of 2 subunits IFN-gamma R1 (ligand binding) and R2 (signal transduction). The expression and proportion of these subunits influences IFN-gamma activity. The aim of the study was to assess the gene expression of IFN-gamma and its receptors in peripheral blood mononuclear cells (PBMC) from patients with syndrome X.
  
  
  METHODS
  The study was carried out in 36 patients aged 44-77 (average 57 years old) with cardiac syndrome X and 23 sex- and age-matched healthy subjects (control group). To evaluate gene expression of IFNgamma and its receptor total mRNA was extracted from peripheral blood mononuclear cells (PBMC) and the number of mRNA copies were assessed by quantitive reverse transcriptase polymerase chain reaction (QRT-PCR).
  
  
  RESULTS
  We have not observed statistically significant differences in INFgamma gene expression between studied group and control. Genes encoding IFNgamma receptor subunits showed higher expression in PBMCs from patients with cardiac syndrome X vs control subjects (IFNgammaR1, 97,244 +/- 26,956 c/microg vs 12,120 +/- 2,940 c/microg, p < 0.005, respectively and IFNgammaR2, 129,153 +/- 36,883 c/microg vs 16,445 +/- 2,923 c/microg, p < 0.005, respectively).
  
  
  CONCLUSIONS
  Variation in transcriptional activity of genes encoding INF-gamma receptor subunits may affect function of microvasculature and thereby participate in the pathology of cardiac syndrome X.
authors.affiliation: Department of Cardiology, Medical University of Silesia, Ziolowa 47, 40-635, Katowice, Poland.
authors.forename: Jozefa
authors.initials: J
authors.lastname: Dabek
authors.forename: Andrzej
authors.initials: A
authors.lastname: Kulach
authors.forename: Tadeusz
authors.initials: T
authors.lastname: Wilczok
authors.forename: Urszula
authors.initials: U
authors.lastname: Mazurek
authors.forename: Daniel
authors.initials: D
authors.lastname: Jakubowski
authors.forename: Zbigniew
authors.initials: Z
authors.lastname: Gasior
mesh_terms: D000328:Adult; D000368:Aged; D005260:Female; D015870:Gene Expression / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D007371:Interferon-gamma / Q000235:genetics*; D007963:Leukocytes, Mononuclear / Q000502:physiology; D008297:Male; D017566:Microvascular Angina / Q000276:immunology* / Q000503:physiopathology*; D008875:Middle Aged; D009479:Neuropeptides / Q000502:physiology; D017471:Receptors, Interferon / Q000235:genetics*; D015533:Transcriptional Activation / Q000276:immunology; D000096743:Interferon gamma Receptor
chemical_list: D007371:Interferon-gamma; D009479:Neuropeptides; D017471:Receptors, Interferon; D000096743:Interferon gamma Receptor; C086185:IFNGR2 protein, human; C106428:NocII neuropeptide