Calpain activation and CaMKIV reduction in spinal cords from hSOD1G93A mouse model

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dc.contributor.authorGou Fabregas, Myriam
dc.contributor.authorRamírez-Núñez, Omar
dc.contributor.authorCacabelos Barral, Daniel
dc.contributor.authorBahi i Pla, Núria
dc.contributor.authorPortero Otín, Manuel
dc.contributor.authorGarcera, Ana
dc.contributor.authorSoler i Tatché, Rosa Ma.
dc.date.accessioned2017-01-25T11:19:20Z
dc.date.embargoEndDate2025-01-01
dc.date.issued2014
dc.description.abstractAmyotrophic Lateral Sclerosis (ALS), a severe neurodegenerative disease, affects the upper and lower motor neurons in the brain and spinal cord. In some studies, ALS disease progression has been associatedwith an increase in calcium-dependent degeneration processes.Motoneurons are specifically vulnerable to sustained membrane depolarization and excessive elevation of intracellular calcium concentration. The present study analyzed intracellular events in embryonic motoneurons and adult spinal cords of the hSOD1G93A ALS mouse model. We observed activation of calpain, a calcium-dependent cysteine protease that degrades a variety of substrates, and a reduction in calcium–calmodulin dependent protein kinase type IV (CaMKIV) levels in protein extracts fromspinal cords obtained at several time-points of hSOD1G93A mice disease progression. However, in cultured embryonic motoneurons these differences between controls and hSOD1G93A mutants are not evident. Our results support the hypothesis that age-dependent changes in calcium homeostasis and resulting events, e.g., calpain activation and CaMKIV processing, are involved in ALS pathogenesisca_ES
dc.description.sponsorshipThis work was supported by grants fromtheGENAME (Defining Targets for Therapeutics in SMA) to RMS; from the Instituto de Salud Carlos III, Fondo de Investigaciones Sanitarias [PI11-01047],Generalitat de Catalunya [SGR740], and Consolider-Ingenio 2010 [CSD2007-00020] to RMS. ORN holds a fellowship from the Comissionat de Universitats i Recerca, Departament d'Innovació, Universitats i Empresa de la Generalitat de Catalunya, and Fons Social Europeu. We thank Elaine Lilly, Ph.D. (Writer's First Aid), for the English language revision of the manuscript.ca_ES
dc.identifier.doihttps://doi.org/10.1016/j.mcn.2014.07.002
dc.identifier.idgrec021385
dc.identifier.issn1044-7431
dc.identifier.urihttp://hdl.handle.net/10459.1/59117
dc.language.isoengca_ES
dc.publisherElsevierca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.1016/j.mcn.2014.07.002ca_ES
dc.relation.ispartofMolecular and Cellular Neuroscience, 2014, vol. 61, p. 219–225ca_ES
dc.rights(c) Elsevier Inc, 2014ca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccessca_ES
dc.subject.otherALSca_ES
dc.subject.otherNeurodegenerationca_ES
dc.subject.otherIntracellular calciumca_ES
dc.subject.otherCaMKIVca_ES
dc.subject.otherCalpainca_ES
dc.subject.otherhSOD1G93Aca_ES
dc.titleCalpain activation and CaMKIV reduction in spinal cords from hSOD1G93A mouse modelca_ES
dc.typearticleca_ES
dc.type.versionpublishedVersionca_ES
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