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Cathepsin A contributes to left ventricular remodeling by degrading extracellular superoxide dismutase in mice.
Hohl, Mathias; Mayr, Manuel; Lang, Lisa; Nickel, Alexander G; Barallobre-Barreiro, Javier; Yin, Xiaoke; Speer, Thimoteus; Selejan, Simina-Ramona; Goettsch, Claudia; Erb, Katharina; Fecher-Trost, Claudia; Reil, Jan-Christian; Linz, Benedikt; Ruf, Sven; Hübschle, Thomas; Maack, Christoph; Böhm, Michael; Sadowski, Thorsten; Linz, Dominik.
Afiliación
  • Hohl M; Klinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.
  • Mayr M; King's BHF Centre of Research Excellence, The James Black Centre, London, United Kingdom.
  • Lang L; Klinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.
  • Nickel AG; Klinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.
  • Barallobre-Barreiro J; Universitätsklinikum Würzburg, Deutsches Zentrum für Herzinsuffizienz (DZHI), Comprehensive Heart Failure Center (CHFC), Würzburg, Germany.
  • Yin X; King's BHF Centre of Research Excellence, The James Black Centre, London, United Kingdom.
  • Speer T; King's BHF Centre of Research Excellence, The James Black Centre, London, United Kingdom.
  • Selejan SR; Klinik für Innere Medizin IV, Universität des Saarlandes, Homburg/Saar, Germany.
  • Goettsch C; Klinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.
  • Erb K; Medizinische Fakultät, Medizinische Klinik 1, Kardiologie, Universitätsklinikum, Aachen, Germany.
  • Fecher-Trost C; Klinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.
  • Reil JC; Institut für Experimentelle und Klinische Pharmakologie und Toxikologie Universität des Saarlandes, Homburg/Saar, Germany.
  • Linz B; Klinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.
  • Ruf S; Klinik für Innere Medizin II, Universitäres Herzzentrum, Lübeck, Germany.
  • Hübschle T; Faculty of Health and Medical Sciences, Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
  • Maack C; Sanofi-Aventis Deutschland GmbH, Frankfurt, Germany.
  • Böhm M; Sanofi-Aventis Deutschland GmbH, Frankfurt, Germany.
  • Sadowski T; Klinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.
  • Linz D; Universitätsklinikum Würzburg, Deutsches Zentrum für Herzinsuffizienz (DZHI), Comprehensive Heart Failure Center (CHFC), Würzburg, Germany.
J Biol Chem ; 295(36): 12605-12617, 2020 09 04.
Article en En | MEDLINE | ID: mdl-32647007
In the heart, the serine carboxypeptidase cathepsin A (CatA) is distributed between lysosomes and the extracellular matrix (ECM). CatA-mediated degradation of extracellular peptides may contribute to ECM remodeling and left ventricular (LV) dysfunction. Here, we aimed to evaluate the effects of CatA overexpression on LV remodeling. A proteomic analysis of the secretome of adult mouse cardiac fibroblasts upon digestion by CatA identified the extracellular antioxidant enzyme superoxide dismutase (EC-SOD) as a novel substrate of CatA, which decreased EC-SOD abundance 5-fold. In vitro, both cardiomyocytes and cardiac fibroblasts expressed and secreted CatA protein, and only cardiac fibroblasts expressed and secreted EC-SOD protein. Cardiomyocyte-specific CatA overexpression and increased CatA activity in the LV of transgenic mice (CatA-TG) reduced EC-SOD protein levels by 43%. Loss of EC-SOD-mediated antioxidative activity resulted in significant accumulation of superoxide radicals (WT, 4.54 µmol/mg tissue/min; CatA-TG, 8.62 µmol/mg tissue/min), increased inflammation, myocyte hypertrophy (WT, 19.8 µm; CatA-TG, 21.9 µm), cellular apoptosis, and elevated mRNA expression of hypertrophy-related and profibrotic marker genes, without affecting intracellular detoxifying proteins. In CatA-TG mice, LV interstitial fibrosis formation was enhanced by 19%, and the type I/type III collagen ratio was shifted toward higher abundance of collagen I fibers. Cardiac remodeling in CatA-TG was accompanied by an increased LV weight/body weight ratio and LV end diastolic volume (WT, 50.8 µl; CatA-TG, 61.9 µl). In conclusion, CatA-mediated EC-SOD reduction in the heart contributes to increased oxidative stress, myocyte hypertrophy, ECM remodeling, and inflammation, implicating CatA as a potential therapeutic target to prevent ventricular remodeling.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Superóxido Dismutasa / Remodelación Ventricular / Miocitos Cardíacos / Catepsina A / Proteolisis Límite: Animals Idioma: En Revista: J Biol Chem Año: 2020 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Superóxido Dismutasa / Remodelación Ventricular / Miocitos Cardíacos / Catepsina A / Proteolisis Límite: Animals Idioma: En Revista: J Biol Chem Año: 2020 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos