Mechanism for the differentiation of EoL-1 cells into eosinophils by histone deacetylase inhibitors
- Authors
- Kaneko, Motoko; Ishihara, Kenji; Takahashi, Aki; Hong, JangJa; Hirasawa, Noriyasu; Zee, OkPyo; Ohuchi, Kazuo
- Issue Date
- Jun-2007
- Publisher
- KARGER
- Keywords
- EoL-1 cells; eosinophils; differentiation; histone deacetylase inhibitors; FIP1L1; PDGFRA
- Citation
- INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY, v.143, pp 28 - 32
- Pages
- 5
- Journal Title
- INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY
- Volume
- 143
- Start Page
- 28
- End Page
- 32
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/14992
- DOI
- 10.1159/000101401
- ISSN
- 1018-2438
1423-0097
- Abstract
- Background: EoL-1 cells have a FIP1L1-PDGFRA fusion gene which causes the transformation of eosinophilic precursor cells into leukemia cells. Recently, we suggested that the induction of differentiation of EoL-1 cells into eosinophils by the HDAC inhibitors apicidin and n-butyrate is due to the continuous inhibition of HDACs. However, neither apicidin nor n-butyrate inhibited the expression of FIP1L1-PDGFRA mRNA, although both these inhibitors suppressed cell proliferation. Therefore, in this study, we analyzed whether the levels of FIP1L1-PDGFR alpha protein and phosphorylated-Stat5 involved in the signaling for the proliferation of EoL-1 cells are attenuated by HDAC inhibitors. Methods: EoL-1 cells were incubated in the presence of apicidin, TSA or n-butyrate. FIP1L1-PDGFR alpha and phosphorylated-Stat5 were detected by Western blotting. Results: Treatment of EoL-1 cells with apicidin at 100 nM or n-butyrate at 500 M decreased the levels of FIP1L1-PDGFR alpha protein and phosphorylated-Stat5, while that with trichostatin A at 30 nM did not. Conclusions: The decrease in the level of FIP1L1-PDGFR alpha protein caused by apicidin and n-butyrate might be one of the mechanisms by which EoL-1 cells are induced to differentiate into eosinophils by these HDAC inhibitors. Copyright (C) 2007 S. Karger AG, Basel.
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