Yuanyuan Huang and Fenghua Zhao contributed equally to this work.
Increased expression of histone deacetylases 2 in temporal lobe epilepsy: A study of epileptic patients and rat models
Version of Record online: 3 NOV 2011
Copyright © 2011 Wiley Periodicals, Inc.
Volume 66, Issue 2, pages 151–159, February 2012
How to Cite
Huang, Y., Zhao, F., Wang, L., Yin, H., Zhou, C. and Wang, X. (2012), Increased expression of histone deacetylases 2 in temporal lobe epilepsy: A study of epileptic patients and rat models. Synapse, 66: 151–159. doi: 10.1002/syn.20995
- Issue online: 7 DEC 2011
- Version of Record online: 3 NOV 2011
- Accepted manuscript online: 10 OCT 2011 07:39AM EST
- Manuscript Accepted: 23 SEP 2011
- Manuscript Received: 5 JUL 2011
- National Natural Science Foundation of China. Grant Number: NO30870877
- Chongqing Municipal Education Commission. Grant Number: KJ080307
- histone deacetylases2 (HDAC2);
- temporal lobe epilepsy (TLE);
Histone deacetylases 2 (HDAC2) is expressed in the central nervous system; it has multiple functions in neural plasticity. However, we do not know if HDAC2 is also involved in the pathology of epilepsy. Here we report that HDAC2 was expressed in the brain tissues of both control and temporal lobe epilepsy (TLE) patients. Results from immunofluorescence and immunohistochemistry showed that HDAC2 was primarily located in the nucleus and that TLE patients exhibit significantly more HDAC2 positive cells than control. Western blotting showed that HDAC2 protein levels were significantly higher in TLE than in control brain. Moreover, in the rat model of TLE, there was a sustained enhancement of HDAC2 expression in rat models of TLE. HDAC2 was significantly increased in both the acute (1 day) and chronic (60 days) animals compared with control group. These results suggest that HDAC2 play an important role in the pathogenesis of human TLE. Synapse, 2012. © 2011 Wiley Periodicals, Inc.