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http://hdl.handle.net/2445/197083
Title: | Voltage-dependent Na+ channel phenotype changes in myoblasts. Consequences for cardiac repair |
Author: | Martínez-Mármol, Ramón David, Miren Sanches, Rosario Roura-Ferrer, Meritxell Villalonga, Núria Sorianello, Eleonora Webb, Susan M. Zorzano Olarte, Antonio Gumà i Garcia, Anna Maria Valenzuela, Carmen Felipe Campo, Antonio |
Keywords: | Canals iònics Miogènesi Malalties del cor Biologia del desenvolupament Ion channels Myogenesis Heart diseases Developmental biology |
Issue Date: | 1-Dec-2007 |
Publisher: | Oxford University Press |
Abstract: | 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. |
Note: | Versió postprint del document publicat a: https://doi.org/10.1016/j.cardiores.2007.08.009 |
It is part of: | Cardiovascular Research, 2007, vol. 76, num. 3, p. 430-441 |
URI: | http://hdl.handle.net/2445/197083 |
Related resource: | https://doi.org/10.1016/j.cardiores.2007.08.009 |
ISSN: | 0008-6363 |
Appears in Collections: | Articles publicats en revistes (Bioquímica i Biomedicina Molecular) |
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