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). CONCLUSION: 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.
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). CONCLUSION: 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.
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