Valproic Acid Regulates alpha-Synuclein Expression through JNK Pathway in Rat Primary Astrocytes.
- Author:
Jung Nam KIM
1
;
Min Kyeong KIM
;
Kyu Suk CHO
;
Chang Soon CHOI
;
Seung Hwa PARK
;
Sung Il YANG
;
So Hyun JOO
;
Jin Hee PARK
;
Geonho BAHN
;
Chan Young SHIN
;
He Jin LEE
;
Seol Heui HAN
;
Kyoung Ja KWON
Author Information
1. Department of Neuroscience, School of Medicine, Konkuk University, Seoul 143-701, Republic of Korea. kjjasmine@hanmail.net
- Publication Type:Original Article
- Keywords:
alpha-synuclein;
Valproic acid;
Stability;
JNK;
Neuroprotection;
Acetylation
- MeSH:
Acetylation;
alpha-Synuclein*;
Animals;
Astrocytes*;
MAP Kinase Signaling System*;
Neurons;
Neuroprotective Agents;
Parkinson Disease;
Phosphorylation;
Rats*;
RNA, Messenger;
Valproic Acid*
- From:Biomolecules & Therapeutics
2013;21(3):222-228
- CountryRepublic of Korea
- Language:English
-
Abstract:
Although the role of alpha-synuclein aggregation on Parkinson's disease is relatively well known, the physiological role and the regulatory mechanism governing the expression of alpha-synuclein are unclear yet. We recently reported that alpha-synuclein is expressed and secreted from cultured astrocytes. In this study, we investigated the effect of valproic acid (VPA), which has been suggested to provide neuroprotection by increasing alpha-synuclein in neuron, on alpha-synuclein expression in rat primary astrocytes. VPA concentration-dependently increased the protein expression level of alpha-synuclein in cultured rat primary astrocytes with concomitant increase in mRNA expression level. Likewise, the level of secreted alpha-synuclein was also increased by VPA. VPA increased the phosphorylation of Erk1/2 and JNK and pretreatment of a JNK inhibitor SP600125 prevented the VPA-induced increase in alpha-synuclein. Whether the increased alpha-synuclein in astrocytes is involved in the reported neuroprotective effects of VPA awaits further investigation.
