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Analysis of myocardial cellular gene expression during pressure overload reveals matrix based functional intercellular communication.
Froese, Natali; Cordero, Julio; Abouissa, Aya; Trogisch, Felix A; Grein, Steve; Szaroszyk, Malgorzata; Wang, Yong; Gigina, Anna; Korf-Klingebiel, Mortimer; Bosnjak, Berislav; Davenport, Colin F; Wiehlmann, Lutz; Geffers, Robert; Riechert, Eva; Jürgensen, Lonny; Boileau, Etienne; Lin, Yanzhu; Dieterich, Christoph; Förster, Reinhold; Bauersachs, Johann; Ola, Roxana; Dobreva, Gergana; Völkers, Mirko; Heineke, Joerg.
Afiliación
  • Froese N; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany.
  • Cordero J; Department of Anatomy and Developmental Biology, European Center for Angioscience (ECAS), Medical Faculty Mannheim of Heidelberg University, 68167 Mannheim, Germany.
  • Abouissa A; Department of Cardiovascular Physiology, European Center for Angioscience (ECAS), Medical Faculty Mannheim of Heidelberg University, Ludolf-Krehl-Str. 7-11, 68167 Mannheim, Germany.
  • Trogisch FA; Department of Cardiovascular Physiology, European Center for Angioscience (ECAS), Medical Faculty Mannheim of Heidelberg University, Ludolf-Krehl-Str. 7-11, 68167 Mannheim, Germany.
  • Grein S; Department of Cardiovascular Physiology, European Center for Angioscience (ECAS), Medical Faculty Mannheim of Heidelberg University, Ludolf-Krehl-Str. 7-11, 68167 Mannheim, Germany.
  • Szaroszyk M; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany.
  • Wang Y; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany.
  • Gigina A; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany.
  • Korf-Klingebiel M; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany.
  • Bosnjak B; Institute of Immunology, 30625 Hannover, Germany.
  • Davenport CF; Research Core Unit Genomics, Hannover Medical School, 30625 Hannover, Germany.
  • Wiehlmann L; Research Core Unit Genomics, Hannover Medical School, 30625 Hannover, Germany.
  • Geffers R; Genome Analytics, Helmholtz Center for Infection Research, 38124 Braunschweig, Germany.
  • Riechert E; Department of Internal Medicine III, Medical Faculty of Heidelberg, University of Heidelberg, 69120 Heidelberg, Germany.
  • Jürgensen L; Department of Internal Medicine III, Medical Faculty of Heidelberg, University of Heidelberg, 69120 Heidelberg, Germany.
  • Boileau E; Department of Internal Medicine III, Medical Faculty of Heidelberg, University of Heidelberg, 69120 Heidelberg, Germany.
  • Lin Y; German Center for Cardiovascular Research (DZHK), Partner Site Heidelberg/Mannheim, 69120 Heidelberg, Germany.
  • Dieterich C; Section of Bioinformatics and Systems Cardiology, Klaus Tschira Institute for Integrative Computational Cardiology, 69120 Heidelberg, Germany.
  • Förster R; Department of Experimental Pharmacology, European Center for Angioscience (ECAS), Medical Faculty Mannheim of Heidelberg University, 68167 Mannheim, Germany.
  • Bauersachs J; Department of Internal Medicine III, Medical Faculty of Heidelberg, University of Heidelberg, 69120 Heidelberg, Germany.
  • Ola R; German Center for Cardiovascular Research (DZHK), Partner Site Heidelberg/Mannheim, 69120 Heidelberg, Germany.
  • Dobreva G; Section of Bioinformatics and Systems Cardiology, Klaus Tschira Institute for Integrative Computational Cardiology, 69120 Heidelberg, Germany.
  • Völkers M; Institute of Immunology, 30625 Hannover, Germany.
  • Heineke J; Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany.
iScience ; 25(3): 103965, 2022 Mar 18.
Article en En | MEDLINE | ID: mdl-35281736
To identify cellular mechanisms responsible for pressure overload triggered heart failure, we isolated cardiomyocytes, endothelial cells, and fibroblasts as most abundant cell types from mouse hearts in the subacute and chronic stages after transverse aortic constriction (TAC) and performed RNA-sequencing. We detected highly cell-type specific transcriptional responses with characteristic time courses and active intercellular communication. Cardiomyocytes after TAC exerted an early and sustained upregulation of inflammatory and matrix genes and a concomitant suppression of metabolic and ion channel genes. Fibroblasts, in contrast, showed transient early upregulation of inflammatory and matrix genes and downregulation of angiogenesis genes, but sustained induction of cell cycle and ion channel genes during TAC. Endothelial cells transiently induced cell cycle and extracellular matrix genes early after TAC, but exerted a long-lasting upregulation of inflammatory genes. As we found that matrix production by multiple cell types triggers pathological cellular responses, it might serve as a future therapeutic target.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: IScience Año: 2022 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos
Texto completo
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Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: IScience Año: 2022 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos