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Título
In vitro aging promotes endoplasmic reticulum (ER)-mitochondria Ca2+ cross talk and loss of store-operated Ca2+ entry (SOCE) in rat hippocampal neurons
Año del Documento
2016
Editorial
Elsevier
Descripción
Producción Científica
Documento Fuente
Biochim Biophys Acta Mol Cel Res 1863(11): 2637-2649
Résumé
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 ERmitochondria
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 becomeoverloaded, 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 ERmitochondrial
cross talking and loss of SOCE. This subcellular Ca2+ remodeling might contribute to cognitive decline
and susceptibility to neuron cell death in the elderly.
Materias (normalizadas)
Hippocampal neurons
ISSN
1388-1981
Revisión por pares
SI
Patrocinador
Ministerio de Economía y Competitividad (BFU2012-37146 and BFU2015- 70131R)
Junta de Castilla y León (VA145U13 and BIO/VA33/13)
Junta de Castilla y León (VA145U13 and BIO/VA33/13)
Version del Editor
Idioma
eng
Derechos
openAccess
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