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Authordc.contributor.authorAltamirano, Francisco 
Authordc.contributor.authorValladares, Denisse 
Authordc.contributor.authorHenríquez Olguín, Carlos 
Authordc.contributor.authorCasas, Mariana 
Authordc.contributor.authorLópez, Jose R. 
Authordc.contributor.authorAllen, Paul D. 
Authordc.contributor.authorJaimovich Pérez, Enrique 
Cita de ítemdc.identifier.citationPLoS ONE, Volumen 8, Issue 12, 2018,
Abstractdc.description.abstractDuchenne Muscular Dystrophy (DMD) is a recessive X-linked genetic disease, caused by mutations in the gene encoding dystrophin. DMD is characterized in humans and in mdx mice by a severe and progressive destruction of muscle fibers, inflammation, oxidative/nitrosative stress, and cell death. In mdx muscle fibers, we have shown that basal ATP release is increased and that extracellular ATP stimulation is pro-apoptotic. In normal fibers, depolarization-induced ATP release is blocked by nifedipine, leading us to study the potential therapeutic effect of nifedipine in mdx muscles and its relation with extracellular ATP signaling. Acute exposure to nifedipine (10 μM) decreased [Ca 2+]r, NF-κB activity and iNOS expression in mdx myotubes. In addition, 6-week-old mdx mice were treated with daily intraperitoneal injections of nifedipine, 1 mg/Kg for 1 week. This treatment lowered the [Ca2+]r measured in vivo in the mdx vastus lateralis. We demonstrated that extracellular ATP levels were higher
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
Link to Licensedc.rights.uri
Sourcedc.sourcePLoS ONE
Keywordsdc.subjectMedicine (all)
Keywordsdc.subjectBiochemistry, Genetics and Molecular Biology (all)
Keywordsdc.subjectAgricultural and Biological Sciences (all)
Títulodc.titleNifedipine treatment reduces resting calcium concentration, oxidative and apoptotic gene expression, and improves muscle function in dystrophic mdx mice
Document typedc.typeArtículo de revista
Indexationuchile.indexArtículo de publicación SCOPUS

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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile