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Institute for Enzyme Research, University of Tokushima, 3-18-15 Kuramoto, Tokushima 770-8503, Japan
¹ Department of Hand Surgery, China-Japan Union Hospital of Jilin University, 126 Xiantai St, Changchun 130031, China

(Requests for offprints should be addressed to K Tsuchida; Email: tsuchida{at}ier.tokushima-u.ac.jp)

(Y L Bao is now at Institute of Genetics and Cytology, Northeast Normal University, 5268 Renmin St, Changchun 130024, China)
(T Matsuzaki is now at Department of Biology, Faculty of Sciences, Kyushu University Graduate School, Fukuoka 812-8581, Japan)

Activin has previously been shown to act as a nerve cell survival factor and to have neurotrophic effects on neurons. However, the role of activin in regulating neurotransmitter expression in the central nervous system and the exact mechanisms involved in this process are poorly understood. In the present study, we report that activin A and basic fibroblast growth factor (bFGF) synergistically increased the protein level of tyrosine hydroxylase (TH), and also greatly increased the TH mRNA level, in both mouse E14 striatal primary cell cultures and the hippocampal neuronal cell line HT22. Activin A and bFGF cooperatively stimulated nuclear translocation of Smad3 and specifically activated ERK1/2, but not p38 or JNK. Interestingly, a specific inhibitor for MEK, U0126, efficiently blocked the induction of TH promoter activity by activin A and bFGF, indicating that activin A collaborated with bFGF signaling to induce the TH gene through selective activation of ERK-type MAP kinase in mouse striatal and HT22 cells. These data suggest that activin A may act in concert with bFGF for the development of TH-positive neurons.

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