Exosome Release Is Modulated by the Mitochondrial-Lysosomal Crosstalk in Parkinson's Disease Stress Conditions.
Exosome release
Mitochondria-lysosome crosstalk
Mitochondrial dysfunctions
Parkinson’s disease
Journal
Molecular neurobiology
ISSN: 1559-1182
Titre abrégé: Mol Neurobiol
Pays: United States
ID NLM: 8900963
Informations de publication
Date de publication:
Apr 2021
Apr 2021
Historique:
received:
21
04
2020
accepted:
02
12
2020
pubmed:
7
1
2021
medline:
28
10
2021
entrez:
6
1
2021
Statut:
ppublish
Résumé
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra (SN) pars compacta region of the brain. The main pathological hallmark involves cytoplasmic inclusions of α-synuclein and mitochondrial dysfunction, which is observed in other part of the central nervous system other than SN suggesting the spread of pathogenesis to bystander neurons. The inter-neuronal communication through exosomes may play an important role in the spread of the disease; however, the mechanisms are not well elucidated. Mitochondria and its role in inter-organellar crosstalk with multivesicular body (MVB) and lysosome and its role in modulation of exosome release in PD is not well understood. In the current study, we investigated the mitochondria-lysosome crosstalk modulating the exosome release in neuronal and glial cells. We observed that PD stress showed enhanced release of exosomes in dopaminergic neurons and glial cells. The PD stress condition in these cells showed fragmented network and mitochondrial dysfunction which further leads to functional deficit of lysosomes and hence inhibition of autophagy flux. Neuronal and glial cells treated with rapamycin showed enhanced autophagy and inhibited the exosomal release. The results here suggest that maintenance of mitochondrial function is important for the lysosomal function and hence exosomal release which is important for the pathogenesis of PD.
Identifiants
pubmed: 33404982
doi: 10.1007/s12035-020-02243-3
pii: 10.1007/s12035-020-02243-3
doi:
Substances chimiques
Sirolimus
W36ZG6FT64
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1819-1833Subventions
Organisme : Department of Biotechnology , Ministry of Science and Technology
ID : BT/PR19937/MED/122/17/2016
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