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JDP2 overexpression provokes cardiac dysfunction in mice.
Heger, Jacqueline; Bornbaum, Julia; Würfel, Alona; Hill, Christian; Brockmann, Nils; Gáspár, Renáta; Pálóczi, János; Varga, Zoltán V; Sárközy, Márta; Bencsik, Péter; Csont, Tamás; Török, Szilvia; Kojonazarov, Baktybek; Schermuly, Ralph Theo; Böngler, Kerstin; Parahuleva, Mariana; Ferdinandy, Peter; Schulz, Rainer; Euler, Gerhild.
Afiliación
  • Heger J; Institute of Physiology, Justus Liebig University, Giessen, Germany.
  • Bornbaum J; Institute of Physiology, Justus Liebig University, Giessen, Germany.
  • Würfel A; Institute of Physiology, Justus Liebig University, Giessen, Germany.
  • Hill C; Institute of Physiology, Justus Liebig University, Giessen, Germany.
  • Brockmann N; Institute of Physiology, Justus Liebig University, Giessen, Germany.
  • Gáspár R; Department of Biochemistry, University of Szeged, Szeged, Hungary.
  • Pálóczi J; Department of Biochemistry, University of Szeged, Szeged, Hungary.
  • Varga ZV; Pharmahungary Group, Szeged, Hungary.
  • Sárközy M; Department of Biochemistry, University of Szeged, Szeged, Hungary.
  • Bencsik P; Department of Biochemistry, University of Szeged, Szeged, Hungary.
  • Csont T; Department of Biochemistry, University of Szeged, Szeged, Hungary.
  • Török S; Pharmahungary Group, Szeged, Hungary.
  • Kojonazarov B; Department of Biochemistry, University of Szeged, Szeged, Hungary.
  • Schermuly RT; Department of Biochemistry, University of Szeged, Szeged, Hungary.
  • Böngler K; Universities of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardio-Pulmonary System (ECCPS), Member of the German Center for Lung Research (DZL), Giessen, Germany.
  • Parahuleva M; Universities of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardio-Pulmonary System (ECCPS), Member of the German Center for Lung Research (DZL), Giessen, Germany.
  • Ferdinandy P; Institute of Physiology, Justus Liebig University, Giessen, Germany.
  • Schulz R; Internal Medicine/Cardiology and Angiology, University Hospital of Giessen and Marburg, Location Marburg, Marburg, Germany.
  • Euler G; Department of Biochemistry, University of Szeged, Szeged, Hungary.
Sci Rep ; 8(1): 7647, 2018 05 16.
Article en En | MEDLINE | ID: mdl-29769710
The transcriptional regulator JDP2 (Jun dimerization protein 2) has been identified as a prognostic marker for patients to develop heart failure after myocardial infarction. We now performed in vivo studies on JDP2-overexpressing mice, to clarify the impact of JDP2 on heart failure progression. Therefore, during birth up to the age of 4 weeks cardiac-specific JDP2 overexpression was prevented by doxycycline feeding in transgenic mice. Then, JDP2 overexpression was started. Already after 1 week, cardiac function, determined by echocardiography, decreased which was also resembled on the cardiomyocyte level. After 5 weeks blood pressure declined, ejection fraction and cardiac output was reduced and left ventricular dilatation developed. Heart weight/body weight, and mRNA expression of ANP, inflammatory marker genes, collagen and fibronectin increased. Collagen 1 protein expression increased, and fibrosis developed. As an additional sign of elevated extracellular matrix remodeling, matrix metalloproteinase 2 activity increased in JDP2 mice. Thus, JDP2 overexpression is deleterious to heart function in vivo. It can be concluded that JDP2 overexpression provokes cardiac dysfunction in adult mice that is accompanied by hypertrophy and fibrosis. Thus, induction of JDP2 is a maladaptive response contributing to heart failure development.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteínas Represoras / Fibrosis / Cardiomegalia / Miocitos Cardíacos / Insuficiencia Cardíaca / Infarto del Miocardio Tipo de estudio: Etiology_studies / Prognostic_studies Límite: Animals Idioma: En Revista: Sci Rep Año: 2018 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteínas Represoras / Fibrosis / Cardiomegalia / Miocitos Cardíacos / Insuficiencia Cardíaca / Infarto del Miocardio Tipo de estudio: Etiology_studies / Prognostic_studies Límite: Animals Idioma: En Revista: Sci Rep Año: 2018 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Reino Unido