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The signals of FGFs on the neurogenesis of embryonic stem cells

Ching-Wen Chen1, Chin-San Liu2, Ing-Ming Chiu3, Shih-Cheng Shen1, Hung-Chuan Pan4, Kun-Hsiung Lee5, Shinn-Zong Lin6 and Hong-Lin Su17*

Author Affiliations

1 Department of Life Sciences, National Chung-Hsing University, Taichung, Taiwan

2 Department of Medical Research, Changhua Christian Hospital, Changhua, Taiwan

3 Institute of Cellular and Systems Medicine, National Health Research Institutes; Miaoli, Taiwan

4 Department of Neurosurgery, Taichung Veterans General Hospital; Taichung, Taiwan

5 Animal Technology Institute Taiwan; Miaoli, Taiwan

6 Center for Neuropsychiatry, China Medical University and Hospital, Taichung, Taiwan; China Medical University Beigang Hospital, Yunlin, Taiwan; Department of Immunology, China Medical University, Taichung, Taiwan

7 Department of Physical Therapy, China Medical University, Taichung, Taiwan

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Journal of Biomedical Science 2010, 17:33  doi:10.1186/1423-0127-17-33

Published: 29 April 2010



Neural induction is a complex process and the detailed mechanism of FGF-induced neurogenesis remains unclear.


By using a serum-free neural induction method, we showed that FGF1 dose-dependently promoted the induction of Sox1/N-cadherin/nestin triple positive cells, which represent primitive neuroblasts, from mouse embryonic stem (ES) cells.


We demonstrated that FGF1, FGF2, and FGF4, but not FGF8b, enhanced this neurogenesis. Especially, FGF-enhanced neurogenesis is not mediated through the rescue of the apoptosis or the enhancement of the proliferation of Sox1+ cells. We further indicated that the inactivation of c-Jun N-terminal kinase-1 (JNK-1) and extracellular signal-related kinase-2 (ERK-2), but not p38 mitogen-activated protein kinase (MAPK), inhibited the neural formation through the inhibition of ES differentiation, but not through the formation of endomesodermal cells.


These lines of evidence delineated the roles of FGF downstream signals in the early neural differentiation of ES cells.