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Vol. 143, Suppl. 1, 2007
Issue release date: June 2007
Section title: Original Paper
Int Arch Allergy Immunol 2007;143:28–32
(DOI:10.1159/000101401)

Mechanism for the Differentiation of EoL-1 Cells into Eosinophils by Histone Deacetylase Inhibitors

Kaneko M. · Ishihara K. · Takahashi A. · Hong J. · Hirasawa N. · Zee O. · Ohuchi K.
aLaboratory of Pathophysiological Biochemistry, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan; bLaboratory of Pharmacognosy, Graduate School of Pharmacy, Sungkyunkwan University, Suwon, Korea and cLaboratory of Pathophysiology, College of Pharmacy, Sookmyung Women’s University, Seoul, Korea; dFaculty of Pharmacy, Yasuda Woman’s University, Hiroshima, Japan

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: 5/31/2007

Number of Print Pages: 5
Number of Figures: 2
Number of Tables: 1

ISSN: 1018-2438 (Print)
eISSN: 1423-0097 (Online)

For additional information: http://www.karger.com/IAA

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-PDGFRα 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-PDGFRα and phosphorylated-Stat5 were detected by Western blotting. Results: Treatment of EoL-1 cells with apicidin at 100 nM or n-butyrate at 500 µM decreased the levels of FIP1L1-PDGFRα protein and phosphorylated-Stat5, while that with trichostatin A at 30 nM did not. Conclusions: The decrease in the level of FIP1L1-PDGFRα 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.


  

Author Contacts

Correspondence to: Dr. Kenji Ishihara
Laboratory of Pathophysiological Biochemistry
Graduate School of Pharmaceutical Sciences, Tohoku University
6-3 Aoba Aramaki, Aoba-ku, Sendai, Miyagi 980-8578 (Japan)
Tel. +81 22 795 6862, Fax +81 22 795 6863, E-Mail ishihara@mail.pharm.tohoku.ac.jp

  

Article Information

Published online: May 31, 2007
Number of Print Pages : 5
Number of Figures : 2, Number of Tables : 1, Number of References : 26

  

Publication Details

International Archives of Allergy and Immunology

Vol. 143, No. Suppl. 1, Year 2007 (Cover Date: June 2007)

Journal Editor: Valenta, R. (Vienna)
ISSN: 1018–2438 (print), 1423–0097 (Online)

For additional information: http://www.karger.com/IAA


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: 5/31/2007

Number of Print Pages: 5
Number of Figures: 2
Number of Tables: 1

ISSN: 1018-2438 (Print)
eISSN: 1423-0097 (Online)

For additional information: http://www.karger.com/IAA


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