RT info:eu-repo/semantics/article
T1 In vitro aging promotes endoplasmic reticulum (ER)-mitochondria Ca2 + cross talk and loss of store-operated Ca2 + entry (SOCE) in rat hippocampal neurons
A1 Calvo Rodríguez, María
A1 García Durillo, Mónica
A1 Villalobos Jorge, Carlos
A1 Núñez Llorente, Lucía
K1 Aging
K1 Envejecimiento
K1 Hippocampal neurons
K1 Neuronas hipocampales
K1 Endoplasmic reticulum
K1 Retículo endoplasmático
K1 Mitochondria
K1 Mitocondrias
AB 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.
PB Elsevier
SN 0167-4889
YR 2016
FD 2016
LK http://uvadoc.uva.es/handle/10324/45043
UL http://uvadoc.uva.es/handle/10324/45043
LA eng
NO Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2016, vol. 1863, n. 11. p. 2637-2649
NO Producción Científica
DS UVaDOC
RD 03-jun-2024