dc.contributor.author | Calvo Rodríguez, María | |
dc.contributor.author | García Durillo, Mónica | |
dc.contributor.author | Villalobos Jorge, Carlos | |
dc.contributor.author | Núñez Llorente, Lucía | |
dc.date.accessioned | 2021-01-18T10:34:31Z | |
dc.date.available | 2021-01-18T10:34:31Z | |
dc.date.issued | 2016 | |
dc.identifier.citation | Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2016, vol. 1863, n. 11. p. 2637-2649 | es |
dc.identifier.issn | 0167-4889 | es |
dc.identifier.uri | http://uvadoc.uva.es/handle/10324/45043 | |
dc.description | Producción Científica | es |
dc.description.abstract | Aging 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.mimetype | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | Elsevier | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/ | * |
dc.subject.classification | Aging | es |
dc.subject.classification | Envejecimiento | es |
dc.subject.classification | Hippocampal neurons | es |
dc.subject.classification | Neuronas hipocampales | es |
dc.subject.classification | Endoplasmic reticulum | es |
dc.subject.classification | Retículo endoplasmático | es |
dc.subject.classification | Mitochondria | es |
dc.subject.classification | Mitocondrias | es |
dc.title | In vitro aging promotes endoplasmic reticulum (ER)-mitochondria Ca2 + cross talk and loss of store-operated Ca2 + entry (SOCE) in rat hippocampal neurons | es |
dc.type | info:eu-repo/semantics/article | es |
dc.rights.holder | © 2016 Elsevier | es |
dc.identifier.doi | 10.1016/j.bbamcr.2016.08.001 | es |
dc.relation.publisherversion | https://www.sciencedirect.com/science/article/pii/S0167488916302051?via%3Dihub | es |
dc.peerreviewed | SI | es |
dc.description.project | Ministerio de Economía, Industria y Competitividad (grants BFU2012-37146 and BFU2015-70131R) | es |
dc.description.project | Junta de Castilla y León (grants VA145U13 and BIO/VA33/13) | es |
dc.rights | Attribution-NonCommercial-NoDerivs 3.0 Unported | * |
dc.type.hasVersion | info:eu-repo/semantics/publishedVersion | es |
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