Neuronal Differentiation of Neuro 2a Cells by Inhibitors of Cell Cycle Progression, Trichostatin A and Butyrolactone I

Trichostatin A (TSA, 17 nM), a specific and reversible inhibitor of histone deacetylase induced neurite network formation at and after 4 days. The networks were preserved for at least 3 weeks in the presence of TSA. Butyrolactone I (BLI, 23.6 μM), an inhibitor of cdc2 and cdk2 kinases, also induced...

Full description

Saved in:
Bibliographic Details
Published in:Biochemical and biophysical research communications 1999-03, Vol.256 (2), p.372-376
Main Authors: Inokoshi, Junji, Katagiri, Masako, Arima, Shiho, Tanaka, Haruo, Hayashi, Masahiko, Bae Kim, Young, Furumai, Ryohei, Yoshida, Minoru, Horinouchi, Sueharu, Ōmura, Satoshi
Format: Article
Language:English
Subjects:
4-Butyrolactone - analogs & derivatives
4-Butyrolactone - pharmacology
Acetylcholinesterase - metabolism
Animals
Blotting, Western
Cell Cycle - drug effects
Cell Differentiation - drug effects
Cell Size - drug effects
Cyclin-Dependent Kinase Inhibitor p21
Cyclin-Dependent Kinases - antagonists & inhibitors
Cyclin-Dependent Kinases - metabolism
Cyclins - metabolism
DNA - biosynthesis
Enzyme Activation - drug effects
Enzyme Inhibitors - pharmacology
Flow Cytometry
Histone Deacetylase Inhibitors
Histone Deacetylases - metabolism
Histones - metabolism
Hydroxamic Acids - pharmacology
Immunohistochemistry
Mice
Neurites - drug effects
Neurites - metabolism
Neurons - cytology
Neurons - drug effects
Tumor Cells, Cultured
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Trichostatin A (TSA, 17 nM), a specific and reversible inhibitor of histone deacetylase induced neurite network formation at and after 4 days. The networks were preserved for at least 3 weeks in the presence of TSA. Butyrolactone I (BLI, 23.6 μM), an inhibitor of cdc2 and cdk2 kinases, also induced neurite extension. Both compounds enhanced the acetylcholinesterase activity of the cells. Cell cycle progression of the cells was blocked by TSA (17 nM) at G1 phase alone. Furthermore, the level of histone hyperacetylation and p21WAF1expression in TSA-treated cells increased transiently. These findings suggest that the induction of the neuronal differentiation in Neuro 2a cells by these agents requires the cell cycle arrest at G1 phase, which is caused by inhibition of cycline dependent kinase, a target molecule of BLI and p21WAF1.
ISSN:0006-291X
1090-2104
DOI:10.1006/bbrc.1999.0316