Your browser doesn't support javascript.
loading
A Possible Role of Tetrodotoxin-Sensitive Na+ Channels for Oxidation-Induced Late Na+ Currents in Cardiomyocytes.
Schneider, Anja; Hage, Axel; Stein, Inês Carvalheira Arnaut Pombeiro; Kriedemann, Nils; Zweigerdt, Robert; Leffler, Andreas.
Afiliación
  • Schneider A; Department of Anesthesiology and Intensive Care Medicine, Hannover Medical School, 30625 Hannover, Germany.
  • Hage A; Department of Anesthesiology and Intensive Care Medicine, Hannover Medical School, 30625 Hannover, Germany.
  • Stein ICAP; Department of Anesthesiology and Intensive Care Medicine, Hannover Medical School, 30625 Hannover, Germany.
  • Kriedemann N; Leibniz Research Laboratories for Biotechnology and Artificial Organs (LEBAO), Department of Cardiothoracic, Transplantation and Vascular Surgery (HTTG), REBIRTH-Research Center for Translational Regenerative Medicine, Hannover Medical School, 30625 Hannover, Germany.
  • Zweigerdt R; Leibniz Research Laboratories for Biotechnology and Artificial Organs (LEBAO), Department of Cardiothoracic, Transplantation and Vascular Surgery (HTTG), REBIRTH-Research Center for Translational Regenerative Medicine, Hannover Medical School, 30625 Hannover, Germany.
  • Leffler A; Department of Anesthesiology and Intensive Care Medicine, Hannover Medical School, 30625 Hannover, Germany.
Int J Mol Sci ; 25(12)2024 Jun 15.
Article en En | MEDLINE | ID: mdl-38928302
ABSTRACT
An accumulation of reactive oxygen species (ROS) in cardiomyocytes can induce pro-arrhythmogenic late Na+ currents by removing the inactivation of voltage-gated Na+ channels including the tetrodotoxin (TTX)-resistant cardiac α-subunit Nav1.5 as well as TTX-sensitive α-subunits like Nav1.2 and Nav1.3. Here, we explored oxidant-induced late Na+ currents in mouse cardiomyocytes and human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) as well as in HEK 293 cells expressing Nav1.2, Nav1.3, or Nav1.5. Na+ currents in mouse cardiomyocytes and hiPSC-CMs treated with the oxidant chloramine T (ChT) developed a moderate reduction in peak current amplitudes accompanied by large late Na+ currents. While ChT induced a strong reduction in peak current amplitudes but only small persistent currents on Nav1.5, both Nav1.2 and Nav1.3 produced increased peak current amplitudes and large persistent currents following oxidation. TTX (300 nM) blocked ChT-induced late Na+ currents significantly stronger as compared to peak Na+ currents in both mouse cardiomyocytes and hiPSC-CMs. Similar differences between Nav1.2, Nav1.3, and Nav1.5 regarding ROS sensitivity were also evident when oxidation was induced with UVA-light (380 nm) or the cysteine-selective oxidant nitroxyl (HNO). To conclude, our data on TTX-sensitive Na+ channels expressed in cardiomyocytes may be relevant for the generation of late Na+ currents following oxidative stress.
Asunto(s)
Palabras clave
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Oxidación-Reducción / Tetrodotoxina / Miocitos Cardíacos / Células Madre Pluripotentes Inducidas Límite: Animals / Humans Idioma: En Revista: Int J Mol Sci Año: 2024 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Oxidación-Reducción / Tetrodotoxina / Miocitos Cardíacos / Células Madre Pluripotentes Inducidas Límite: Animals / Humans Idioma: En Revista: Int J Mol Sci Año: 2024 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Suiza