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Valproate recovers the inhibitory effect of dexamethasone on the proliferation of the adult dentate gyrus-derived neural precursor cells via GSK-3 beta and beta-catenin pathway

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/56639

Title: Valproate recovers the inhibitory effect of dexamethasone on the proliferation of the adult dentate gyrus-derived neural precursor cells via GSK-3 beta and beta-catenin pathway
Authors: Boku, Shuken Browse this author →KAKEN DB
Nakagawa, Shin Browse this author →KAKEN DB
Masuda, Takahiro Browse this author
Nishikawa, Hiroyuki Browse this author
Kato, Akiko Browse this author
Takamura, Naoki Browse this author
Omiya, Yuki Browse this author
Kitaichi, Yuji Browse this author
Inoue, Takeshi Browse this author →KAKEN DB
Kusumi, Ichiro Browse this author →KAKEN DB
Keywords: Neurogenesis
Glucocorticoid
Mood disorder
Mood stabilizer
Hippocampus
Issue Date: 15-Jan-2014
Publisher: Elsevier science bv
Journal Title: European journal of pharmacology
Volume: 723
Start Page: 425
End Page: 430
Publisher DOI: 10.1016/j.ejphar.2013.10.060
PMID: 24211784
Abstract: Neurogenesis in the adult dentate gyrus (DC) is decreased in rodent models for mood disorders. Mood stabilizers including lithium (Li) and valproate (VPA) increase it. These increasing effects of Li and VPA on neurogenesis in adult DG are considered to be one of the therapeutic actions of Li and VPA, but their molecular mechanism remains unclear. We have already reported that Li recovers the inhibitory effects of dexamethasone (DEX), an agonist of glucocorticoid receptor, on the proliferation of adult rat DG-derived neural precursor cells (ADP) via GSK-3 beta and beta-catenin pathway. Following it, here we investigated the mechanism underlying the recovery effects of VPA on DEX-induced decrease of ADP proliferation. VPA is an inhibitor of histone deacetylase (HDAC). However, Trichostatin A, a HDAC inhibitor, had no effect on ADP proliferation. In contrast, SB415286, a specific GSK-3 beta inhibitor, recovered DEX-induced decrease of ADP proliferation. In addition, quercetin (Que), a beta-catenin pathway inhibitor, abolished such a recovery effect of VPA. Moreover, nuclear p-catenin and the expression of cyclin D1 were altered by DEX. VPA and Que like the proliferation. Moreover, VPA increased the phosphorylation of Ser(9), which is known as the inhibitory phosphorylation site of GSK-3 beta. These suggest that HDAC is not involved in the recovery effect of VPA on ADP proliferation and that VPA recovers the inhibitory effects of DEX via increasing the phosphorylation of Ser9 on GsK-3 beta and following up-regulation of beta-catenin pathway. Therefore, GSK-3 beta and beta-catenin pathway might play a role in the increasing effects of VPA on neurogenesis on adult DC. (C) 2013 Elsevier B.V. All rights reserved,
Type: article (author version)
URI: http://hdl.handle.net/2115/56639
Appears in Collections:北海道大学病院 (Hokkaido University Hospital) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 朴 秀賢

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