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dc.contributor.authorMecha, Miriam-
dc.contributor.authorTorrao, Andrea S.-
dc.contributor.authorMestre, Leyre-
dc.contributor.authorCarrillo-Salinas, F. J.-
dc.contributor.authorMechoulam, Raphael-
dc.contributor.authorGuaza, Carmen-
dc.date.accessioned2012-11-15T15:15:24Z-
dc.date.available2012-11-15T15:15:24Z-
dc.date.issued2012-06-28-
dc.identifierdoi: 10.1038/cddis.2012.71-
dc.identifierissn: 2041-4889-
dc.identifier.citationCell Death & Disease 3: e331 (2012)-
dc.identifier.urihttp://hdl.handle.net/10261/60355-
dc.description.abstractCannabidiol (CBD) is the most abundant cannabinoid in Cannabis sativa that has no psychoactive properties. CBD has been approved to treat inflammation, pain and spasticity associated with multiple sclerosis (MS), of which demyelination and oligodendrocyte loss are hallmarks. Thus, we investigated the protective effects of CBD against the damage to oligodendrocyte progenitor cells (OPCs) mediated by the immune system. Doses of 1 μM CBD protect OPCs from oxidative stress by decreasing the production of reactive oxygen species. CBD also protects OPCs from apoptosis induced by LPS/IFNγ through the decrease of caspase 3 induction via mechanisms that do not involve CB1, CB2, TRPV1 or PPARc receptors. Tunicamycin-induced OPC death was attenuated by CBD, suggesting a role of endoplasmic reticulum (ER) stress in the mode of action of CBD. This protection against ER stress-induced apoptosis was associated with reduced phosphorylation of eiF2α, one of the initiators of the ER stress pathway. Indeed, CBD diminished the phosphorylation of PKR and eiF2α induced by LPS/IFNγ. The pro-survival effects of CBD in OPCs were accompanied by decreases in the expression of ER apoptotic effectors (CHOP, Bax and caspase 12), and increased expression of the anti-apoptotic Bcl-2. These findings suggest that attenuation of the ER stress pathway is involved in the 'oligoprotective' effects of CBD during inflammation. © 2012 Macmillan Publishers Limited All rights reserved.-
dc.description.sponsorshipWe acknowledge the financial support of the Ministry of Science and Innovation (MICINN, project SAF-2010/17501), Instituto de Salud Carlos III (project RD07/0060/0010 RETICS program, Red Española de Esclerosis Múltiple, REEM). Mecha M is supported by REEM.-
dc.language.isoeng-
dc.publisherNature Publishing Group-
dc.rightsopenAccess-
dc.titleCannabidiol protects oligodendrocyte progenitor cells from inflammation-induced apoptosis by attenuating endoplasmic reticulum stress-
dc.typeartículo-
dc.identifier.doi10.1038/cddis.2012.71-
dc.relation.publisherversionhttp://doi.org/10.1038/cddis.2012.71-
dc.date.updated2012-11-15T15:15:24Z-
dc.description.versionPeer Reviewed-
dc.rights.licensehttp://creativecommons.org/licenses/by-nc-nd/3.0/-
dc.contributor.funderMinisterio de Ciencia e Innovación (España)-
dc.contributor.funderInstituto de Salud Carlos III-
dc.contributor.funderRed Española de Esclerosis Múltiple-
dc.contributor.funderRedes Temáticas de Investigación Cooperativa en Salud (España)-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004837es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100007747es_ES
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