Effect of quinolinic acid on gene expression in human astrocytes

Implications for Alzheimer's disease

Ka Ka Ting, Bruce J. Brew, Gilles J. Guillemin*

*Corresponding author for this work

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Activated microglia and astrocytes play a key role in the neuroinflammatory response during Alzheimer's disease (AD). The kynurenine pathway (KP) of tryptophan degradation is activated and production of the excitotoxin quinolinic acid (QUIN) by monocytic cells is increased. We studied here the effects of QUIN in pathophysiological concentrations on the expression of genes including IL-1β, IL-6, S100β, Glutamate synthetase (GS) glial fibrillary acidic protein (GFAP) that are commonly associated with astrocytes in the development of neuroinflammation in AD. We found that IL-6, S100β and GS genes were constitutively expressed in human adult astrocytes (HAA) and only with TNFα, but not QUIN, IL-6 and S100β expression were increased compared with controls in HAA. IL-1β expression was increased by IFN-γ, TNFα and QUIN in HAA. These preliminary results suggest that QUIN's role in astroglial inflammatory response is mediated by increase of IL-1β expression. Therefore, QUIN is likely to play a role in astroglial inflammatory response that may contribute to the pathogenesis of AD.

Original languageEnglish
Pages (from-to)384-388
Number of pages5
JournalInternational Congress Series
Volume1304
DOIs
Publication statusPublished - 1 Nov 2007
Externally publishedYes

Keywords

  • Alzheimer's disease
  • GFAP
  • GS
  • Human adult astrocytes
  • IFNγ
  • IL-6
  • IL1β
  • Inflammation
  • Kynurenine pathway
  • Quinolinic acid
  • S100β
  • TNFα

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