GSK3β mediates the induced expression of synaptic acetylcholinesterase during apoptosis

Peng Jing, Qihuang Jin, Jun Wu, Xue Jun Zhang

Research output: Contribution to journalArticle

20 Scopus citations

Abstract

Besides its role in terminating acetylcholine-mediated neurotransmission, acetylcholinesterase (AChE) is found to be expressed and participate in the process of apoptosis in various cell types. However, the mechanisms underlying AChE up-regulation in neuronal cells remain elusive. Herein we demonstrated that glycogen synthase kinase-3β (GSK3β) mediates induced AChE-S expression during apoptosis. In this study, A23187 and thapsigargin (TG) were employed to induce apoptosis in neuroendocrine PC12 cells. The results showed that exposure of PC12 cells to A23187 and TG up-regulated AChE activity significantly. The same treatment also led to activation of GSK3β. Two different inhibitors of GSK3β (lithium and GSK3β-specific inhibitor VIII) could block A23187- or TG-induced up-regulation of AChE activity, AChE-S mRNA level and protein expression. However, lithium could not inhibit the induction of AChE-R mRNA and protein under similar conditions. Taken together, our results show that GSK3β is specifically involved in the induction of AChE-S expression in PC12 cells during apoptosis.

Original languageEnglish (US)
Pages (from-to)409-419
Number of pages11
JournalJournal of Neurochemistry
Volume104
Issue number2
DOIs
StatePublished - Jan 2008

Keywords

  • A23187
  • Acetylcholinesterase
  • Apoptosis
  • Glycogen synthase kinase-3β
  • PC12 cells
  • Thapsigargin

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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