Skip to main content
Log in

Transcriptional Activity of Genes Encoding Interferon γ (IFNγ) and its Receptor Assessed in Peripheral Blood Mononuclear Cells in Patients with Cardiac Syndrome X

  • Published:
Inflammation Aims and scope Submit manuscript

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.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Fig. 1

Similar content being viewed by others

References

  1. Kemp, H. G. 1973. Left ventricular function in patients with the anginal syndrome and normal coronary angiograms. Am. J. Cardiol. 32:375–376.

    Article  PubMed  Google Scholar 

  2. Panting, J. R., P. D. Gatehause, G. Z. Yang, and F. Grothues. 2002. Abnormal subendocardial perfusion in cardiac syndrome X detected by cardiovascular magnetic resonance imaging. N. Engl. J. Med. 346:1948–1953.

    Article  PubMed  Google Scholar 

  3. Tymińska-Sędek K., and M. Jakubowska-Najnigier. 2002., Chory z kardiologicznym zespołem X. Terapia. 9(2):41–47.

    Google Scholar 

  4. Rogacka D., and H. Wysocki. 2003. Dławica mikronaczyniowa i zaburzenia percepcji bólu jako główne składowe patogenetyczne kardiologicznego zespołu X. Folia Cardiol. 10:553–561.

    Google Scholar 

  5. Kaski J. C., G. M. Rosano, and P. Collins. 1995. Cardiac syndrome X: Clinical characteristics and left ventricular function long-term follow-up study. JACC 25:807–814.

    PubMed  CAS  Google Scholar 

  6. Johnson B. D. et al. 2004. Prognosis in women with myocardial ischemia in the absence of obstructive coronary disease: results from the National Institutes of Health–National Heart, Lung, and Blood Institutes-sponsored Women’s Ischemia Syndrome Evaluation (WISE). Circulation 109:2993–2999.

    Article  PubMed  Google Scholar 

  7. Kołodziej K., and J. D. Kasprzak. 2001. Kardiologiczny zespół X. Forum Kardiol. 4:1425–3674.

    Google Scholar 

  8. Vazquez-Rey E., and J. C. Kaski. 2003. Cardiovascular syndrome X and endothelial dysfunction. Rev. Esp. Cardiol. 56:181–192.

    Article  PubMed  Google Scholar 

  9. Leu H. B., C. P. Lin, W. T. Lin, T. C. Wu, S. J. Lin, and J. W, Chen. 2006. Circulating mononuclear superoxide production and inflammatory markers for long-term prognosis in patients with cardiac syndrome X. Free Radic. Biol. Med. 40:983–991.

    Article  PubMed  CAS  Google Scholar 

  10. Zhang P., Z. Chen, F. Chen, M. Li, J. Fan, H. Zhou, J. Liu, and Z. Huang. 2004. Expression of IFN-γ and its receptor alpha in the peripheral blood of patients with chronic hepatitis C. Chin. Med. J. 117(1):79–82.

    PubMed  CAS  Google Scholar 

  11. Deb, D. K., A. Sassano, F. Lekmine, B. Majchrzak, A. Verma, S. Kambhampat, S. Uddin, A. Rahman, E. N. Fis, and L. C. Platanias. 2003. Activation of Protein Kinase CD by IFN. J. Immunol. 171:267–273.

    PubMed  CAS  Google Scholar 

  12. Allione A., P. Bernabei, M. Bosticardo, S. Ariotti, S. Forni, and F. Novell. 1999. Nitric oxide suppresses human T lymphocyte proliferation through IFN-γ-dependent and IFN-γ-independent induction of apoptosis. J. Immunol. 163:4182–4191.

    PubMed  CAS  Google Scholar 

  13. Pestka, S. 1997. The interferon receptors. Semin. Oncol. 24:S9–18–S9–40 (Jun).

    Google Scholar 

  14. Haus O. 2000. The genes of interferons and interferon-related factors: Localization and relationships with chromosome aberrations in cancer. Arch. Immunol. Ther. Exp. 48:95–100.

    CAS  Google Scholar 

  15. Robertson B., X. J. Xu, J. X. Hao, Z. Wiesenfeld-Hallin, J. Mhlanga, G. Grant, and K. Kristensson. 1997. Interferon-gamma receptors in nociceptive pathways: role in neuropathic pain-related behaviour. NeuroReport. 8:1311–1316.

    Article  PubMed  CAS  Google Scholar 

  16. Fernandes J. L., R. L. Mamoni, J. L. Orford, C. Garcia, A. P. Selwyn, O. R. Coelho, and M. H. Blotta. 2004. Increased Th1 activity in patients with coronary artery disease. Cytokine. 26(3):131–137 (May 7).

    Article  PubMed  CAS  Google Scholar 

  17. Reiss A. B., C. A. Patel, M. M. Rahman, E. S. Chan, K. Hasneen, M. C. Montesinos, J. D. Trachman, and B. N. Cronstein. 2004. Interferon-gamma impedes reverse cholesterol transport and promotes foam cell transformation in THP-1 human monocytes/macrophages. Med. Sci. Monit. 10:BR420–BR425.

    PubMed  CAS  Google Scholar 

  18. Inagaki Y., S. Yamagishi, S. Amano, T. Okamoto, K. Koga, and Z. Makita. 2002. Interferon-gamma-induced apoptosis and activation of THP-1 macrophages. Life Sci. 71:2499–2508.

    Article  PubMed  CAS  Google Scholar 

  19. Koh K. P., Y. Wang, T. Yi, S. L. Shiao, M. I. Lorber, W. C. Sessa, G. Tellides, and J. S. Pober. 2004. T cell-mediated vascular dysfunction of human allografts results from IFN-γ dysregulation of NO synthase. J. Clin. Invest. 114:846–856, September 15.

    Article  PubMed  CAS  Google Scholar 

  20. Lin C. P., W. T. Lin, H. B. Leu, T. C. Wu, and J. W. Chen. 2003. Differential mononuclear cell activity and endothelial inflammation in coronary artery disease and cardiac syndrome X. Int. J. Cardiol. 89:53–62.

    Article  PubMed  Google Scholar 

  21. Hartrick C. T. 2002. Increased production of nitric oxide stimulated by interferon-gamma from peripheral blood monocytes in patients with complex regional pain syndrome. Neurosci Lett. 323:75–77.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Andrzej Kulach.

Rights and permissions

Reprints and permissions

About this article

Cite this article

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

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s10753-007-9028-0

Key words

Navigation