Recombinant pro-CTSD (cathepsin D) enhances SNCA/α-Synuclein degradation in α-Synucleinopathy models.
alpha-synuclein
cathepsin D
lysosomal degradation
lysosomal storage disorders
parkinson disease
synucleinopathies
Journal
Autophagy
ISSN: 1554-8635
Titre abrégé: Autophagy
Pays: United States
ID NLM: 101265188
Informations de publication
Date de publication:
05 2022
05 2022
Historique:
pubmed:
16
3
2022
medline:
14
6
2022
entrez:
15
3
2022
Statut:
ppublish
Résumé
Parkinson disease (PD) is a neurodegenerative disorder characterized by the abnormal intracellular accumulation of SNCA/α-synuclein. While the exact mechanisms underlying SNCA pathology are not fully understood, increasing evidence suggests the involvement of autophagy as well as lysosomal deficiencies. Because CTSD (cathepsin D) has been proposed to be the major lysosomal protease involved in SNCA degradation, its deficiency has been linked to the presence of insoluble SNCA conformers in the brain of mice and humans as well as to the transcellular transmission of SNCA aggregates. We here postulate that SNCA degradation can be enhanced by the application of the recombinant human proform of CTSD (rHsCTSD). Our results reveal that rHsCTSD is efficiently endocytosed by neuronal cells, correctly targeted to lysosomes and matured to an enzymatically active protease. In dopaminergic neurons derived from induced pluripotent stem cells (iPSC) of PD patients harboring the A53T mutation within the
Identifiants
pubmed: 35287553
doi: 10.1080/15548627.2022.2045534
pmc: PMC9196656
doi:
Substances chimiques
Amyloid beta-Peptides
0
SNCA protein, human
0
Snca protein, mouse
0
alpha-Synuclein
0
CTSD protein, human
EC 3.4.23.5
Cathepsin D
EC 3.4.23.5
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1127-1151Subventions
Organisme : NINDS NIH HHS
ID : R01 NS092823
Pays : United States
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