Protective Function of STAT3 in CVB3-Induced Myocarditis. (24th May 2012)

• Record Type: Journal Article
• Authors: Lindner, Diana; Hilbrandt, Moritz; Marggraf, Katharina; Becher, P. Moritz; Hilfiker-Kleiner, Denise; Klingel, Karin; Pauschinger, Matthias; Schultheiss, Heinz-Peter; Tschöpe, Carsten; Westermann, Dirk
• Other Names: Giamouzis Gregory Academic Editor.
• Is Part Of: Cardiology research and practice. Volume 2012(2012)
• Publication Date: 2012-05-24
• Subjects: Cardiology -- Research -- Periodicals; Cardiology -- Periodicals; Cardiology; Cardiology; Cardiology -- Research; Electronic journals; Periodicals; Periodicals; 616.12
• DOI: 10.1155/2012/437623
• Languages: English
• ISSNs: 2090-8016

Abstract

Abstract : The transcription factor signal transducer and activator of transcription 3 (STAT3) is an important mediator of the inflammatory process. We investigated the role of STAT3 in viral myocarditis and its possible role in the development to dilated cardiomyopathy. We used STAT3-deficent mice with a cardiomyocyte-restricted knockout and induced a viral myocarditis using Coxsackievirus B3 (CVB3) which induced a severe inflammation during the acute phase of the viral myocarditis. A complete virus clearance and an attenuated inflammation were examined in both groups WT and STAT3 KO mice 4 weeks after infection, but the cardiac function in STAT3 KO mice was significantly decreased in contrast to the infected WT mice. Interestingly, an increased expression of collagen I was detected in STAT3 KO mice compared to WT mice 4 weeks after CVB3 infection. Furthermore, the matrix degradation was reduced in STAT3 KO mice which might be an explanation for the observed matrix deposition. Consequently, we here demonstrate the protective function of STAT3 in CVB3-induced myocarditis. Since the cardiomyocyte-restricted knockout leads to an increased fibrosis, it can be assumed that STAT3 signalling in cardiomyocytes protects the heart against increased fibrosis through paracrine effects.