Mechanism for the differentiation of EoL-1 cells into eosinophils by histone deacetylase inhibitors

Motoko Kaneko, Kenji Ishihara, Aki Takahashi, Jang Ja Hong, Noriyasu Hirasawa, Ok Pyo Zee, Kazuo Ohuchi

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)28-32
Number of pages5
JournalInternational archives of allergy and immunology
Volume143
Issue numberSUPPL. 1
DOIs
Publication statusPublished - 2007 Jun 1

Keywords

  • Differentiation
  • EoL-1 cells
  • Eosinophils
  • FIP1L1-PDGFRA
  • Histone deacetylase inhibitors

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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