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Pink1/Parkin deficiency alters circulating lymphocyte populations and increases platelet-T cell aggregates in rats
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Pink1/Parkin deficiency alters circulating lymphocyte populations and increases platelet-T cell aggregates in rats
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Journal Article
Pink1/Parkin deficiency alters circulating lymphocyte populations and increases platelet-T cell aggregates in rats
2024
Overview
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.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ Animals
/ B cells
/ Blood Platelets - metabolism
/ CD8-Positive T-Lymphocytes - immunology
/ CD8-Positive T-Lymphocytes - metabolism
/ Humanities and Social Sciences
/ Kinases
/ Leukocytes, Mononuclear - metabolism
/ Male
/ Mutation
/ Neurons
/ Parkin
/ Parkinson Disease - genetics
/ Parkinson Disease - metabolism
/ Parkinson Disease - pathology
/ Peripheral blood mononuclear cells
/ Pink1
/ Protein Kinases - deficiency
/ Protein Kinases - metabolism
/ Proteins
/ Protons
/ PTEN-induced putative kinase
/ Rats
/ Science
/ T cells
/ Ubiquitin-Protein Ligases - deficiency
