Pink1/Parkin deficiency alters circulating lymphocyte populations and increases platelet-T cell aggregates in rats.
Animals
Ubiquitin-Protein Ligases
/ metabolism
Protein Kinases
/ metabolism
Rats
Blood Platelets
/ metabolism
Mitochondria
/ metabolism
Parkinson Disease
/ genetics
Male
Glycolysis
T-Lymphocytes
/ metabolism
CD8-Positive T-Lymphocytes
/ metabolism
Leukocytes, Mononuclear
/ metabolism
Platelet Aggregation
B cells
Energetics
Parkin
Pink1
Platelets
T cells
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
11 Oct 2024
11 Oct 2024
Historique:
received:
16
05
2024
accepted:
30
09
2024
medline:
12
10
2024
pubmed:
12
10
2024
entrez:
11
10
2024
Statut:
epublish
Résumé
Parkinson's disease (PD) is the most common progressive neurodegenerative movement disorder and results from the selective loss of dopaminergic neurons in the substantia nigra pars compacta. Pink1 and Parkin are proteins that function together in mitochondrial quality control, and when they carry loss-of-function mutations lead to familial forms of PD. While much research has focused on central nervous system alterations in PD, peripheral contributions to PD pathogenesis are increasingly appreciated. We report Pink1/Parkin regulate glycolytic and mitochondrial oxidative metabolism in peripheral blood mononuclear cells (PBMCs) from rats. Pink1/Parkin deficiency induces changes in the circulating lymphocyte populations, namely increased CD4 + T cells and decreased CD8 + T cells and B cells. Loss of Pink1/Parkin leads to elevated platelet counts in the blood and increased platelet-T cell aggregation. Platelet-lymphocyte aggregates are associated with increased thrombosis risk suggesting targeting the Pink1/Parkin pathway in the periphery might have therapeutic potential.
Identifiants
pubmed: 39394439
doi: 10.1038/s41598-024-74775-w
pii: 10.1038/s41598-024-74775-w
doi:
Substances chimiques
Ubiquitin-Protein Ligases
EC 2.3.2.27
parkin protein
EC 2.3.2.27
PTEN-induced putative kinase
EC 2.7.11.1
Protein Kinases
EC 2.7.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
23861Subventions
Organisme : NIH HHS
ID : P20GM130447
Pays : United States
Informations de copyright
© 2024. The Author(s).
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