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dc.contributor.authorCalvo Rodríguez, María
dc.contributor.authorGarcía Durillo, Mónica
dc.contributor.authorVillalobos Jorge, Carlos
dc.contributor.authorNúñez Llorente, Lucía 
dc.date.accessioned2021-01-18T10:34:31Z
dc.date.available2021-01-18T10:34:31Z
dc.date.issued2016
dc.identifier.citationBiochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2016, vol. 1863, n. 11. p. 2637-2649es
dc.identifier.issn0167-4889es
dc.identifier.urihttp://uvadoc.uva.es/handle/10324/45043
dc.descriptionProducción Científicaes
dc.description.abstractAging is associated to cognitive decline and susceptibility to neuron death, two processes related recently to subcellular Ca2+ homeostasis. Memory storage relies on mushroom spines stability that depends on store-operated Ca2 + entry (SOCE). In addition, Ca2+ transfer from endoplasmic reticulum (ER) to mitochondria sustains energy production but mitochondrial Ca2+ overload promotes apoptosis. We have addressed whether SOCE and ER-mitochondria Ca2+ transfer are influenced by culture time in long-term cultures of rat hippocampal neurons, a model of neuronal aging. We found that short-term cultured neurons show large SOCE, low Ca2+ store content and no functional coupling between ER and mitochondria. In contrast, in long-term cultures reflecting aging neurons, SOCE is essentially lost, Stim1 and Orai1 are downregulated, Ca2+ stores become overloaded, Ca2+ release is enhanced, expression of the mitochondrial Ca2+ uniporter (MCU) increases and most Ca2 + released from the ER is transferred to mitochondria. These results suggest that neuronal aging is associated to increased ER-mitochondrial cross talking and loss of SOCE. This subcellular Ca2+ remodeling might contribute to cognitive decline and susceptibility to neuron cell death in the elderly.es
dc.format.mimetypeapplication/pdfes
dc.language.isoenges
dc.publisherElsevieres
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/*
dc.subject.classificationAginges
dc.subject.classificationEnvejecimientoes
dc.subject.classificationHippocampal neuronses
dc.subject.classificationNeuronas hipocampaleses
dc.subject.classificationEndoplasmic reticulumes
dc.subject.classificationRetículo endoplasmáticoes
dc.subject.classificationMitochondriaes
dc.subject.classificationMitocondriases
dc.titleIn vitro aging promotes endoplasmic reticulum (ER)-mitochondria Ca2 + cross talk and loss of store-operated Ca2 + entry (SOCE) in rat hippocampal neuronses
dc.typeinfo:eu-repo/semantics/articlees
dc.rights.holder© 2016 Elsevieres
dc.identifier.doi10.1016/j.bbamcr.2016.08.001es
dc.relation.publisherversionhttps://www.sciencedirect.com/science/article/pii/S0167488916302051?via%3Dihubes
dc.peerreviewedSIes
dc.description.projectMinisterio de Economía, Industria y Competitividad (grants BFU2012-37146 and BFU2015-70131R)es
dc.description.projectJunta de Castilla y León (grants VA145U13 and BIO/VA33/13)es
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Unported*
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersiones


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