Abstract:
:Neuroinflammation is involved in the pathogenesis of Parkinson's disease (PD) and other neurodegenerative disorders. We show that lack of PINK1- a mitochondrial kinase linked to recessive familial PD - leads to glia type-specific abnormalities of innate immunity. PINK1 loss enhances LPS/IFN-γ stimulated pro-inflammatory phenotypes of mixed astrocytes/microglia (increased iNOS, nitric oxide and COX-2, reduced IL-10) and pure astrocytes (increased iNOS, nitric oxide, TNF-α and IL-1β), while attenuating expression of both pro-inflammatory (TNF-α, IL-1β) and anti-inflammatory (IL-10) cytokines in microglia. These abnormalities are associated with increased inflammation-induced NF-κB signaling in astrocytes, and cause enhanced death of neurons co-cultured with inflamed PINK1 -/- mixed glia and neuroblastoma cells exposed to conditioned medium from LPS/IFN-γ treated PINK1 -/- mixed glia. Neuroblastoma cell death is prevented with an iNOS inhibitor, implicating increased nitric oxide production as the cause for enhanced death. Finally, we show for the first time that lack of a recessive PD gene (PINK1) increases α-Synuclein-induced nitric oxide production in all glia types (mixed glia, astrocytes and microglia). Our results describe a novel pathogenic mechanism in recessive PD, where PINK1 deficiency may increase neuron death via exacerbation of inflammatory stimuli-induced nitric oxide production and abnormal innate immune responses in glia cells.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Sun L,Shen R,Agnihotri SK,Chen Y,Huang Z,Büeler Hdoi
10.1038/s41598-017-18786-wsubject
Has Abstractpub_date
2018-01-10 00:00:00pages
383issue
1issn
2045-2322pii
10.1038/s41598-017-18786-wjournal_volume
8pub_type
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