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Mol. Cells 2011; 31(2): 159-164

Published online December 22, 2011

https://doi.org/10.1007/s10059-011-0019-5

© The Korean Society for Molecular and Cellular Biology

A Critical Time Window for the Survival of Neural Progenitor Cells by HDAC Inhibitors in the Hippocampus

Byung-Woo Kim1, Sera Yang1, Chang Ho Lee2,3,*, and Hyeon Son1,3,*

1Department of Biochemistry and Molecular Biology, Hanyang University, Seoul 133-791, Korea, 2Department of Pharmacology, College of Medicine, Hanyang University, Seoul 133-791, Korea, 3Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul 133-791, Korea

Correspondence to : *Correspondence: jennysue@hanyang.ac.kr (CHL); hyeonson@hanyang.ac.kr (HS)

Received: September 13, 2010; Revised: October 29, 2010; Accepted: November 10, 2010

Abstract

Histone deacetylase inhibitors (HDACIs) that modulate gene expression by inhibiting HDAC enzymes may contribute to the survival of immature hippocampal neurons. However, it remains unknown how and when HDACIs regulate the survival of newly generated immature hippocampal neurons. In the present study, if the treatment of valproic acid (VPA) and sodium butyrate (SBt) in the specific time window during the development of newly generated neurons resulted in the increased survival of bromodeoxyuridine (BrdU)(+) neurons in the dentate gyrus (DG) of hippocampus in mice was investigated. It was found that the number of BrdU(+) cells, the expressions of anti-apoptotic Bcl-2 family members and pCREB were increased by HDACIs when HDACIs were treated no later than 2-3 weeks after BrdU labeling. This suggests that epigenetic modification within a specific time window is critical for the survival of newborn hippocampal neurons by inhibiting the apoptotic pathway.

Keywords HDAC, neurogenesis, survival, valproate

Article

Research Article

Mol. Cells 2011; 31(2): 159-164

Published online February 28, 2011 https://doi.org/10.1007/s10059-011-0019-5

Copyright © The Korean Society for Molecular and Cellular Biology.

A Critical Time Window for the Survival of Neural Progenitor Cells by HDAC Inhibitors in the Hippocampus

Byung-Woo Kim1, Sera Yang1, Chang Ho Lee2,3,*, and Hyeon Son1,3,*

1Department of Biochemistry and Molecular Biology, Hanyang University, Seoul 133-791, Korea, 2Department of Pharmacology, College of Medicine, Hanyang University, Seoul 133-791, Korea, 3Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul 133-791, Korea

Correspondence to:*Correspondence: jennysue@hanyang.ac.kr (CHL); hyeonson@hanyang.ac.kr (HS)

Received: September 13, 2010; Revised: October 29, 2010; Accepted: November 10, 2010

Abstract

Histone deacetylase inhibitors (HDACIs) that modulate gene expression by inhibiting HDAC enzymes may contribute to the survival of immature hippocampal neurons. However, it remains unknown how and when HDACIs regulate the survival of newly generated immature hippocampal neurons. In the present study, if the treatment of valproic acid (VPA) and sodium butyrate (SBt) in the specific time window during the development of newly generated neurons resulted in the increased survival of bromodeoxyuridine (BrdU)(+) neurons in the dentate gyrus (DG) of hippocampus in mice was investigated. It was found that the number of BrdU(+) cells, the expressions of anti-apoptotic Bcl-2 family members and pCREB were increased by HDACIs when HDACIs were treated no later than 2-3 weeks after BrdU labeling. This suggests that epigenetic modification within a specific time window is critical for the survival of newborn hippocampal neurons by inhibiting the apoptotic pathway.

Keywords: HDAC, neurogenesis, survival, valproate

Mol. Cells
Nov 30, 2023 Vol.46 No.11, pp. 655~725
COVER PICTURE
Kim et al. (pp. 710-724) demonstrated that a pathogen-derived Ralstonia pseudosolanacearum type III effector RipL delays flowering time and enhances susceptibility to bacterial infection in Arabidopsis thaliana. Shown is the RipL-expressing Arabidopsis plant, which displays general dampening of the transcriptional program during pathogen infection, grown in long-day conditions.

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