2026-04-19T11:40:48Zhttps://recercat.cat/oai/request
oai:recercat.cat:2445/1970832025-12-04T21:15:14Zcom_2072_1057col_2072_478781col_2072_478917
RECERCAT author Martínez-Mármol, Ramón author David, Miren author Sanches, Rosario author Roura-Ferrer, Meritxell author Villalonga, Núria author Sorianello, Eleonora author Webb, Susan M. author Zorzano Olarte, Antonio author Gumà i Garcia, Anna Maria author Valenzuela, Carmen author Felipe Campo, Antonio 2023-04-21T07:56:28Z2023-04-21T07:56:28Z2007-12-012023-04-21T07:56:28Z Objective: Cellular cardiomyoplasty using skeletal myoblasts is a promising therapy for myocardial infarct repair. Once transplanted, myoblasts grow, differentiate and adapt their electrophysiological properties towards more cardiac-like phenotypes. Voltage-dependent Na + channels (Na v ) are the main proteins involved in the propagation of the cardiac action potential, and their phenotype affects cardiac performance. Therefore, we examined the expression of Na v during proliferation and differentiation in skeletal myocytes. Methods and results: We used the rat neonatal skeletal myocyte cell line L6E9. Proliferation of L6E9 cells induced Na v 1.4 and Na v 1.5, although neither protein has an apparent role in cell growth. During myogenesis, Na v1.5 was largely induced. Electrophysiological and pharmacological properties, as well as mRNA expression, indicate that cardiac-type Na v1.5 accounts for almost 90% of the Na + current in myotubes. Unlike in proliferation, this protein plays a pivotal role in myogenesis. The adoption of a cardiac-like phenotype is further supported by the increase in Nav 1.5 colocalization in caveolae. Finally, we demonstrate that the treatment of myoblasts with neuregulin further increased Na v 1.5 in skeletal myocytes. Conclusion: Our results indicate that skeletal myotubes adopt a cardiac-like phenotype in cell culture conditions and that the expression of Na v1.5 acts as an underlying molecular mechanism. (c) European Society of Cardiology, 2007 info:eu-repo/semantics/openAccess Canals iònics Miogènesi Malalties del cor Biologia del desenvolupament Ion channels Myogenesis Heart diseases Developmental biology Voltage-dependent Na+ channel phenotype changes in myoblasts. Consequences for cardiac repair info:eu-repo/semantics/article info:eu-repo/semantics/acceptedVersion