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Comparative study of the roles of cytokines and apoptosis in dilated and hypertrophic cardiomyopathies
1 Department of Medical Microbiology and Immunobiology; University of Szeged, Dóm tér 10, H-6720 Szeged, Hungary
2 Second Department of Internal Medicine and Cardiological Center; University of Szeged, Korányi fasor 6, H-6720 Szeged, Hungary
* Corresponding Author: Yvette Mándi,
European Cytokine Network 2004, 15(1), 53-59.
Abstract
Aims. In order to gain more insight into the pathogenesis of dilated and hypertrophic cardiomyo-pathies (DCM and HCM, respectively), we investigated the roles of certain cytokines that regulate apoptosis. Methods and results. ELISA tests, performed to determine the plasma concentrations of tumour necrosis factor-α (TNF-α), the soluble Fas (sFas), interleukin-6 (IL-6) and the soluble IL-6 receptor (sIL-6R), revealed that DCM patients exhibit elevated concentrations of TNF-α, sFas, IL-6 and sIL-6R, while HCM patients have only high IL-6 and sIL-6R levels as compared with healthy individuals. Western blot analysis of the levels of TNF-α, IL-6, Bcl-2 and Bax proteins in myocardium samples demonstrated that DCM patients express increased levels of TNF-α, IL-6 and Bax, whereas HCM heart lysates display only elevated levels of Bcl-2. Annexin V binding assay of TNF-α -treated H9C2 cells indicated that the in vitro cytotoxicity of this cytokine involves apoptotosis and necrosis. Conclusion. In accord with previous observations, our data indicate a strong activation of the pro-apoptotic TNF and Fas pathways in DCM patients, and an anti-apoptotic shift in HCM patients. These findings have a bearing on the pathogenesis of cardiomyopathies, since apoptosis may account for certain dysfunctions observed in DCM, while IL-6 may elicit the hypertrophy characteristic of HCM.Keywords
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Copyright © 2004 The Author(s). Published by Tech Science Press.This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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