α-Synuclein potentiates interleukin-1β-induced CXCL10 expression in human A172 astrocytoma cells

Neda Saffarian Tousi, Daniel J. Buck, Tom Curtis, Randall Davis

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Neuroinflammation and neuronal degeneration observed in Parkinson's disease (PD) has been attributed in part to glial-mediated events. Increased expression of proinflammatory cytokines and abnormal accumulation of the neuronal protein, α-synuclein in the brain are also characteristic of PD. While increasing evidence suggests that astrocytes contribute to neuroinflammation and dopaminergic neuronal degeneration associated with PD, there remains much to learn about these astroglial-mediated events. Therefore, we investigated the in vitro effects of interleukin-1β (IL-1β) and α-synuclein on astroglial expression of interferon-γ inducible protein-10 (CXCL10), a proinflammatory and neurotoxic chemokine. IL-1β-induced CXCL10 protein expression was potentiated by co-exposure to α-synuclein. α-Synuclein did not significantly affect IL-1β-induced CXCL10 mRNA expression, but did mediate increased CXCL10 mRNA stability, which may explain, in part, the increased levels of secreted CXCL10 protein. Future investigations are warranted to more fully define the mechanism by which α-synuclein enhances IL-1β-induced astroglial CXCL10 expression. These findings highlight the importance of α-synuclein in modulating inflammatory events in astroglia. These events may be particularly relevant to the pathology of CNS disorders involving α-synuclein accumulation, including PD and HIV-1 associated dementia.

Original languageEnglish
Pages (from-to)133-136
Number of pages4
JournalNeuroscience Letters
Volume507
Issue number2
DOIs
StatePublished - 24 Jan 2012

Fingerprint

Synucleins
Astrocytoma
Interleukin-1
Parkinson Disease
Astrocytes
Chemokine CXCL10
Proteins
RNA Stability
Chemokines
Neuroglia
Dementia
HIV-1
Pathology
Cytokines
Messenger RNA
Brain

Keywords

  • Astrocyte
  • Chemokine
  • NF-κB
  • Neuroinflammation
  • Parkinson's disease
  • α-Synuclein

Cite this

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title = "α-Synuclein potentiates interleukin-1β-induced CXCL10 expression in human A172 astrocytoma cells",
abstract = "Neuroinflammation and neuronal degeneration observed in Parkinson's disease (PD) has been attributed in part to glial-mediated events. Increased expression of proinflammatory cytokines and abnormal accumulation of the neuronal protein, α-synuclein in the brain are also characteristic of PD. While increasing evidence suggests that astrocytes contribute to neuroinflammation and dopaminergic neuronal degeneration associated with PD, there remains much to learn about these astroglial-mediated events. Therefore, we investigated the in vitro effects of interleukin-1β (IL-1β) and α-synuclein on astroglial expression of interferon-γ inducible protein-10 (CXCL10), a proinflammatory and neurotoxic chemokine. IL-1β-induced CXCL10 protein expression was potentiated by co-exposure to α-synuclein. α-Synuclein did not significantly affect IL-1β-induced CXCL10 mRNA expression, but did mediate increased CXCL10 mRNA stability, which may explain, in part, the increased levels of secreted CXCL10 protein. Future investigations are warranted to more fully define the mechanism by which α-synuclein enhances IL-1β-induced astroglial CXCL10 expression. These findings highlight the importance of α-synuclein in modulating inflammatory events in astroglia. These events may be particularly relevant to the pathology of CNS disorders involving α-synuclein accumulation, including PD and HIV-1 associated dementia.",
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α-Synuclein potentiates interleukin-1β-induced CXCL10 expression in human A172 astrocytoma cells. / Tousi, Neda Saffarian; Buck, Daniel J.; Curtis, Tom; Davis, Randall.

In: Neuroscience Letters, Vol. 507, No. 2, 24.01.2012, p. 133-136.

Research output: Contribution to journalArticle

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