<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-04-13T02:43:15Z</responseDate><request verb="GetRecord" identifier="oai:www.recercat.cat:2445/197083" metadataPrefix="qdc">https://recercat.cat/oai/request</request><GetRecord><record><header><identifier>oai:recercat.cat:2445/197083</identifier><datestamp>2025-12-04T21:15:14Z</datestamp><setSpec>com_2072_1057</setSpec><setSpec>col_2072_478781</setSpec><setSpec>col_2072_478917</setSpec></header><metadata><qdc:qualifieddc xmlns:qdc="http://dspace.org/qualifieddc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://dspace.org/qualifieddc/ http://www.ukoln.ac.uk/metadata/dcmi/xmlschema/qualifieddc.xsd">
   <dc:title>Voltage-dependent Na+ channel phenotype changes in myoblasts. Consequences for cardiac repair</dc:title>
   <dc:creator>Martínez-Mármol, Ramón</dc:creator>
   <dc:creator>David, Miren</dc:creator>
   <dc:creator>Sanches, Rosario</dc:creator>
   <dc:creator>Roura-Ferrer, Meritxell</dc:creator>
   <dc:creator>Villalonga, Núria</dc:creator>
   <dc:creator>Sorianello, Eleonora</dc:creator>
   <dc:creator>Webb, Susan M.</dc:creator>
   <dc:creator>Zorzano Olarte, Antonio</dc:creator>
   <dc:creator>Gumà i Garcia, Anna Maria</dc:creator>
   <dc:creator>Valenzuela, Carmen</dc:creator>
   <dc:creator>Felipe Campo, Antonio</dc:creator>
   <dc:subject>Canals iònics</dc:subject>
   <dc:subject>Miogènesi</dc:subject>
   <dc:subject>Malalties del cor</dc:subject>
   <dc:subject>Biologia del desenvolupament</dc:subject>
   <dc:subject>Ion channels</dc:subject>
   <dc:subject>Myogenesis</dc:subject>
   <dc:subject>Heart diseases</dc:subject>
   <dc:subject>Developmental biology</dc:subject>
   <dcterms: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.</dcterms:abstract>
   <dcterms:issued>2023-04-21T07:56:28Z</dcterms:issued>
   <dcterms:issued>2023-04-21T07:56:28Z</dcterms:issued>
   <dcterms:issued>2007-12-01</dcterms:issued>
   <dcterms:issued>2023-04-21T07:56:28Z</dcterms:issued>
   <dc:type>info:eu-repo/semantics/article</dc:type>
   <dc:type>info:eu-repo/semantics/acceptedVersion</dc:type>
   <dc:relation>Versió postprint del document publicat a: https://doi.org/10.1016/j.cardiores.2007.08.009</dc:relation>
   <dc:relation>Cardiovascular Research, 2007, vol. 76, num. 3, p. 430-441</dc:relation>
   <dc:relation>https://doi.org/10.1016/j.cardiores.2007.08.009</dc:relation>
   <dc:rights>(c) European Society of Cardiology, 2007</dc:rights>
   <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
   <dc:publisher>Oxford University Press</dc:publisher>
   <dc:source>Articles publicats en revistes (Bioquímica i Biomedicina Molecular)</dc:source>
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