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 γ (IFN-γ) is an important cytokine in inflammatory reaction. It acts through its specific receptor composed of 2 subunits
IFN-γ R1 (ligand binding) and R2 (signal transduction). The expression and proportion of these subunits influences IFN-γ activity. The aim of the study was to assess the gene expression of IFN-γ 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 IFNγ 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 INFγ gene expression between studied group and control. Genes encoding IFNγ receptor subunits showed higher expression in PBMCs from patients with cardiac syndrome X vs control subjects (IFNγR1, 97,244 ± 26,956 c/μg vs 12,120 ± 2,940 c/μg, p < 0.005, respectively and IFNγR2, 129,153 ± 36,883 c/μg vs 16,445 ± 2,923 c/μg, p < 0.005, respectively).
Conclusion
Variation in transcriptional activity of genes encoding INF-γ receptor subunits may affect function of microvasculature and thereby participate in the pathology of cardiac syndrome X.
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Dabek, J., Kulach, A., Wilczok, T. et al. Transcriptional Activity of Genes Encoding Interferon γ (IFNγ) and its Receptor Assessed in Peripheral Blood Mononuclear Cells in Patients with Cardiac Syndrome X. Inflammation 30, 125–129 (2007). https://doi.org/10.1007/s10753-007-9028-0
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DOI: https://doi.org/10.1007/s10753-007-9028-0