Table of Contents Author Guidelines Submit a Manuscript
Cardiology Research and Practice
Volume 2012, Article ID 437623, 11 pages
http://dx.doi.org/10.1155/2012/437623
Research Article

Protective Function of STAT3 in CVB3-Induced Myocarditis

1Department of Cardiology and Pneumology, Charité-Universitäts-Medizin Berlin, Campus Benjamin Franklin, 12200 Berlin, Germany
2Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany
3Department of Molecular Pathology, University Hospital, 72076 Tübingen, Germany
4Department of Cardiology, Nuremberg Hospital South, 90471 Nürnberg, Germany

Received 6 February 2012; Accepted 13 March 2012

Academic Editor: Gregory Giamouzis

Copyright © 2012 Diana Lindner et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Linked References

  1. D. Westermann, K. Savvatis, D. Lindner et al., “Reduced degradation of the chemokine MCP-3 by matrix metalloproteinase-2 exacerbates myocardial inflammation in experimental viral cardiomyopathy,” Circulation, vol. 124, no. 19, pp. 2082–2093, 2011. View at Google Scholar
  2. D. Westermann, D. Lindner, M. Kasner et al., “Cardiac inflammation contributes to changes in the extracellular matrix in patients with heart failure and normal ejection fraction,” Circulation, vol. 4, no. 1, pp. 44–52, 2011. View at Publisher · View at Google Scholar · View at Scopus
  3. M. Hazebroek, R. Dennert, and S. Heymans, “Virus infection of the heart—unmet therapeutic needs,” Antiviral Chemistry & Chemotherapy. In press.
  4. H. P. Schultheiss, U. Kuhl, and L. T. Cooper, “The management of myocarditis,” European Heart Journal, vol. 32, no. 21, pp. 2616–2625, 2011. View at Google Scholar
  5. P. Fischer and D. Hilfiker-Kleiner, “Role of gp130-mediated signalling pathways in the heart and its impact on potential therapeutic aspects,” British Journal of Pharmacology, vol. 153, no. 1, pp. S414–S427, 2008. View at Publisher · View at Google Scholar · View at Scopus
  6. D. Hilfiker-Kleiner, A. Hilfiker, and H. Drexler, “Many good reasons to have STAT3 in the heart,” Pharmacology and Therapeutics, vol. 107, no. 1, pp. 131–137, 2005. View at Publisher · View at Google Scholar · View at Scopus
  7. S. Negoro, K. Kunisada, E. Tone et al., “Activation of JAK/STAT pathway transduces cytoprotective signal in rat acute myocardial infarction,” Cardiovascular Research, vol. 47, no. 4, pp. 797–805, 2000. View at Publisher · View at Google Scholar · View at Scopus
  8. S. Hishinuma, M. Funamoto, Y. Fujio, K. Kunisada, and K. Yamauchi-Takihara, “Hypoxic stress induces cardiotrophin-1 expression in cardiac myocytes,” Biochemical and Biophysical Research Communications, vol. 264, no. 2, pp. 436–440, 1999. View at Publisher · View at Google Scholar · View at Scopus
  9. J. Pan, K. Fukuda, H. Kodama et al., “Role of angiotensin II in activation of the JAK/STAT pathway induced by acute pressure overload in the rat heart,” Circulation Research, vol. 81, no. 4, pp. 611–617, 1997. View at Google Scholar · View at Scopus
  10. E. K. Podewski, D. Hilfiker-Kleiner, A. Hilfiker et al., “Alterations in Janus kinase (JAK)-signal transducers and activators of transcription (STAT) signaling in patients with end-stage dilated cardiomyopathy,” Circulation, vol. 107, no. 6, pp. 798–802, 2003. View at Publisher · View at Google Scholar · View at Scopus
  11. T. Tsutamoto, T. Hisanaga, A. Wada et al., “Interleukin-6 spillover in the peripheral circulation increases with the severity of heart failure, and the high plasma level of interleukin-6 is an important prognostic predictor in patients with congestive heart failure,” Journal of the American College of Cardiology, vol. 31, no. 2, pp. 391–398, 1998. View at Publisher · View at Google Scholar · View at Scopus
  12. K. C. Wollert and H. Drexler, “The role of interleukin-6 in the failing heart,” Heart Failure Reviews, vol. 6, no. 2, pp. 95–103, 2001. View at Publisher · View at Google Scholar · View at Scopus
  13. K. Takeda, K. Noguchi, W. Shi et al., “Targeted disruption of the mouse Stat3 gene leads to early embryonic lethality,” Proceedings of the National Academy of Sciences of the United States of America, vol. 94, no. 8, pp. 3801–3804, 1997. View at Publisher · View at Google Scholar · View at Scopus
  14. D. Hilfiker-Kleiner, A. Hilfiker, M. Fuchs et al., “Signal transducer and activator of transcription 3 is required for myocardial capillary growth, control of interstitial matrix deposition, and heart protection from ischemic injury,” Circulation Research, vol. 95, no. 2, pp. 187–195, 2004. View at Publisher · View at Google Scholar · View at Scopus
  15. J. J. Jacoby, A. Kalinowski, M. G. Liu et al., “Cardiomyocyte-restricted knockout of STAT3 results in higher sensitivity to inflammation, cardiac fibrosis, and heart failure with advanced age,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 22, pp. 12929–12934, 2003. View at Publisher · View at Google Scholar · View at Scopus
  16. D. Westermann, B. C. Knollmann, P. Steendijk et al., “Diltiazem treatment prevents diastolic heart failure in mice with familial hypertrophic cardiomyopathy,” European Journal of Heart Failure, vol. 8, no. 2, pp. 115–121, 2006. View at Publisher · View at Google Scholar · View at Scopus
  17. K. Klingel, C. Hohenadl, A. Canu et al., “Ongoing enterovirus-induced myocarditis is associated with persistent heart muscle infection: quantitative analysis of virus replication, tissue damage, and inflammation,” Proceedings of the National Academy of Sciences of the United States of America, vol. 89, no. 1, pp. 314–318, 1992. View at Google Scholar · View at Scopus
  18. R. Kandolf, D. Ameis, P. Kirschner, A. Canu, and P. H. Hofschneider, “In situ detection of enteroviral genomes in myocardial cells by nucleic acid hybridization: an approach to the diagnosis of viral heart disease,” Proceedings of the National Academy of Sciences of the United States of America, vol. 84, no. 17, pp. 6272–6276, 1987. View at Google Scholar · View at Scopus
  19. A. Henke, S. Huber, A. Stelzner, and J. L. Whitton, “The role of CD8+ T lymphocytes in coxsackievirus B3-induced myocarditis,” Journal of Virology, vol. 69, no. 11, pp. 6720–6728, 1995. View at Google Scholar · View at Scopus
  20. R. Kandolf, M. Sauter, C. Aepinus, J. J. Schnorr, H. C. Selinka, and K. Klingel, “Mechanisms and consequences of enterovirus persistence in cardiac myocytes and cells of the immune system,” Virus Research, vol. 62, no. 2, pp. 149–158, 1999. View at Publisher · View at Google Scholar · View at Scopus
  21. D. Hilfiker-Kleiner, A. Limbourg, and H. Drexler, “STAT3-mediated activation of myocardial capillary growth,” Trends in Cardiovascular Medicine, vol. 15, no. 4, pp. 152–157, 2005. View at Publisher · View at Google Scholar · View at Scopus
  22. U. M. Wegenka, J. Buschmann, C. Lutticken, P. C. Heinrich, and F. Horn, “Acute-phase response factor, a nuclear factor binding to acute-phase response elements, is rapidly activated by interleukin-6 at the posttranslational level,” Molecular and Cellular Biology, vol. 13, no. 1, pp. 276–288, 1993. View at Google Scholar · View at Scopus
  23. D. Westermann, M. Kasner, P. Steendijk et al., “Role of left ventricular stiffness in heart failure with normal ejection fraction,” Circulation, vol. 117, no. 16, pp. 2051–2060, 2008. View at Publisher · View at Google Scholar · View at Scopus
  24. M. Kasner, D. Westermann, B. Lopez et al., “Diastolic tissue doppler indexes correlate with the degree of collagen expression and cross-linking in heart failure and normal ejection fraction,” Journal of the American College of Cardiology, vol. 57, no. 8, pp. 977–985, 2011. View at Publisher · View at Google Scholar · View at Scopus
  25. D. Westermann, K. Savvatis, H. P. Schultheiss, and C. Tschöpe, “Immunomodulation and matrix metalloproteinases in viral myocarditis,” Journal of Molecular and Cellular Cardiology, vol. 48, no. 3, pp. 468–473, 2010. View at Publisher · View at Google Scholar · View at Scopus
  26. J. Kukacka, R. Průsa, K. Kotaska, and V. Pelouch, “Matrix metalloproteinases and their function in myocardium,” Biomedical Papers of the Medical Faculty of the University Palacký, Olomouc, Czechoslovakia, vol. 149, no. 2, pp. 225–236, 2005. View at Google Scholar
  27. F. G. Spinale, “Myocardial matrix remodeling and the matrix metalloproteinases: influence on cardiac form and function,” Physiological Reviews, vol. 87, no. 4, pp. 1285–1342, 2007. View at Publisher · View at Google Scholar · View at Scopus
  28. S. L. K. Bowers, I. Banerjee, and T. A. Baudino, “The extracellular matrix: at the center of it all,” Journal of Molecular and Cellular Cardiology, vol. 48, no. 3, pp. 474–482, 2010. View at Publisher · View at Google Scholar · View at Scopus
  29. F. G. Spinale, M. L. Coker, B. R. Bond, and J. L. Zellner, “Myocardial matrix degradation and metalloproteinase activation in the failing heart: a potential therapeutic target,” Cardiovascular Research, vol. 46, no. 2, pp. 225–238, 2000. View at Publisher · View at Google Scholar · View at Scopus
  30. R. Kakkar and R. T. Lee, “Intramyocardial fibroblast myocyte communication,” Circulation Research, vol. 106, no. 1, pp. 47–57, 2010. View at Publisher · View at Google Scholar · View at Scopus
  31. R. D. Brown, S. K. Ambler, M. D. Mitchell, and C. S. Long, “The cardiac fibroblast: therapeutic target in myocardial remodeling and failure,” Annual Review of Pharmacology and Toxicology, vol. 45, pp. 657–687, 2005. View at Publisher · View at Google Scholar · View at Scopus
  32. H. K. Graham, M. Horn, and A. W. Trafford, “Extracellular matrix profiles in the progression to heart failure: European Young Physiologists Symposium Keynote Lecture-Bratislava 2007,” Acta Physiologica, vol. 194, no. 1, pp. 3–21, 2008. View at Publisher · View at Google Scholar · View at Scopus
  33. K. E. Porter and N. A. Turner, “Cardiac fibroblasts: at the heart of myocardial remodeling,” Pharmacology and Therapeutics, vol. 123, no. 2, pp. 255–278, 2009. View at Publisher · View at Google Scholar · View at Scopus
  34. Z. Sheng, K. Knowlton, J. Chen, M. Hoshijima, J. H. Brown, and K. R. Chien, “Cardiotrophin 1 (CT-1) inhibition of cardiac myocyte apoptosis via a mitogen-activated protein kinase-dependent pathway. Divergence from downstream CT-1 signals for myocardial cell hypertrophy,” The Journal of Biological Chemistry, vol. 272, no. 9, pp. 5783–5791, 1997. View at Publisher · View at Google Scholar · View at Scopus
  35. A. Stephanou, B. Brar, R. Heads et al., “Cardiotrophin-1 induces heat shock protein accumulation in cultured cardiac cells and protects them from stressful stimuli,” Journal of Molecular and Cellular Cardiology, vol. 30, no. 4, pp. 849–855, 1998. View at Publisher · View at Google Scholar · View at Scopus
  36. H. Hirota, J. Chen, U. A. K. Betz et al., “Loss of a gp130 cardiac muscle cell survival pathway is a critical event in the onset of heart failure during biomechanical stress,” Cell, vol. 97, no. 2, pp. 189–198, 1999. View at Google Scholar · View at Scopus
  37. K. Kunisada, S. Negoro, E. Tone et al., “Signal transducer and activator of transcription 3 in the heart transduces not only a hypertrophic signal but a protective signal against doxorubicin-induced cardiomyopathy,” Proceedings of the National Academy of Sciences of the United States of America, vol. 97, no. 1, pp. 315–319, 2000. View at Publisher · View at Google Scholar · View at Scopus