Pink1/Parkin deficiency alters circulating lymphocyte populations and increases platelet-T cell aggregates in rats.

Autor:	Manganaro JE; University of Nebraska Medical Center., Emanuel K; University of Nebraska Medical Center., Lamberty BG; University of Nebraska Medical Center., George JW; University of Nebraska Medical Center., Stauch KL; University of Nebraska Medical Center.
Jazyk:	angličtina
Zdroj:	Research square [Res Sq] 2024 May 30. Date of Electronic Publication: 2024 May 30.
DOI:	10.21203/rs.3.rs-4431604/v1
Abstrakt:	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, and venous thrombosis is a cause of sudden death in PD, suggesting targeting the Pink1/Parkin pathway in the periphery has therapeutic potential. Competing Interests: Additional information Conflict-of-interest disclosure: The authors declare no competing or financial interests.
Databáze:	MEDLINE
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