Presenilin-Deficient Neurons and Astrocytes Display Normal Mitochondrial Phenotypes.
Alzheimer's disease
OXPHOS
astrocyte
mitochondria
neuron
presenilins
Journal
Frontiers in neuroscience
ISSN: 1662-4548
Titre abrégé: Front Neurosci
Pays: Switzerland
ID NLM: 101478481
Informations de publication
Date de publication:
2020
2020
Historique:
received:
22
07
2020
accepted:
14
12
2020
entrez:
8
2
2021
pubmed:
9
2
2021
medline:
9
2
2021
Statut:
epublish
Résumé
Presenilin 1 (PS1) and Presenilin 2 (PS2) are predominantly known as the catalytic subunits of the γ-secretase complex that generates the amyloid-β (Aβ) peptide, the major constituent of the senile plaques found in the brain of Alzheimer's disease (AD) patients. Apart from their role in γ-secretase activity, a growing number of cellular functions have been recently attributed to PSs. Notably, PSs were found to be enriched in mitochondria-associated membranes (MAMs) where mitochondria and endoplasmic reticulum (ER) interact. PS2 was more specifically reported to regulate calcium shuttling between these two organelles by controlling the formation of functional MAMs. We have previously demonstrated in mouse embryonic fibroblasts (MEF) an altered mitochondrial morphology along with reduced mitochondrial respiration and increased glycolysis in PS2-deficient cells (PS2KO). This phenotype was restored by the stable re-expression of human PS2. Still, all these results were obtained in immortalized cells, and one bottom-line question is to know whether these observations hold true in central nervous system (CNS) cells. To that end, we carried out primary cultures of PS1 knockdown (KD), PS2KO, and PS1KD/PS2KO (PSdKO) neurons and astrocytes. They were obtained from the same litter by crossing PS2 heterozygous; PS1 floxed (PS2
Identifiants
pubmed: 33551720
doi: 10.3389/fnins.2020.586108
pmc: PMC7862347
doi:
Types de publication
Journal Article
Langues
eng
Pagination
586108Informations de copyright
Copyright © 2021 Contino, Suelves, Vrancx, Vadukul, Payen, Stanga, Bertrand and Kienlen-Campard.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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