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GSK3β mediates the induced expression of synaptic acetylcholinesterase during apoptosis
Author(s) -
Jing Peng,
Jin Qihuang,
Wu Jun,
Zhang XueJun
Publication year - 2008
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2007.04975.x
Subject(s) - acetylcholinesterase , thapsigargin , apoptosis , gsk 3 , aché , microbiology and biotechnology , chemistry , acetylcholine , kinase , medicine , biology , endocrinology , biochemistry , enzyme , extracellular
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.

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