Differentiation of eosinophilic leukemia EoL-1 cells into eosinophils induced by histone deacetylase inhibitors

Life Sci. 2007 Mar 6;80(13):1213-20. doi: 10.1016/j.lfs.2006.12.016. Epub 2007 Jan 11.

Abstract

EoL-1 cells differentiate into eosinophils in the presence of n-butyrate, but the mechanism has remained to be elucidated. Because n-butyrate can inhibit histone deacetylases, we hypothesized that the inhibition of histone deacetylases induces the differentiation of EoL-1 cells into eosinophils. In this study, using n-butyrate and two other histone deacetylase inhibitors, apicidin and trichostatin A, we have analyzed the relationship between the inhibition of histone deacetylases and the differentiation into eosinophils in EoL-1 cells. It was demonstrated that apicidin and n-butyrate induced a continuous acetylation of histones H4 and H3, inhibited the proliferation of EoL-1 cells without attenuating the level of FIP1L1-PDGFRA mRNA, and induced the expression of markers for mature eosinophils such as integrin beta7, CCR1, and CCR3 on EoL-1 cells, while trichostatin A evoked a transient acetylation of histones and induced no differentiation into eosinophils. These findings suggest that the continuous inhibition of histone deacetylases in EoL-1 cells induces the differentiation into mature eosinophils.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylation / drug effects
  • Butyrates / pharmacology
  • Cell Differentiation / drug effects*
  • Cell Proliferation / drug effects
  • Dose-Response Relationship, Drug
  • Enzyme Inhibitors / pharmacology*
  • Eosinophils / drug effects*
  • Eosinophils / enzymology
  • Gene Expression Regulation, Enzymologic / drug effects
  • HL-60 Cells
  • Histone Deacetylase Inhibitors*
  • Histone Deacetylases / metabolism
  • Histones / metabolism
  • Humans
  • Hydroxamic Acids / pharmacology
  • Hypereosinophilic Syndrome / drug therapy*
  • Hypereosinophilic Syndrome / enzymology
  • Peptides, Cyclic / pharmacology
  • Platelet-Derived Growth Factor / genetics
  • Platelet-Derived Growth Factor / metabolism
  • RNA, Messenger / metabolism
  • mRNA Cleavage and Polyadenylation Factors / genetics
  • mRNA Cleavage and Polyadenylation Factors / metabolism

Substances

  • Butyrates
  • Enzyme Inhibitors
  • FIP1L1 protein, human
  • Histone Deacetylase Inhibitors
  • Histones
  • Hydroxamic Acids
  • Peptides, Cyclic
  • Platelet-Derived Growth Factor
  • RNA, Messenger
  • apicidin
  • mRNA Cleavage and Polyadenylation Factors
  • trichostatin A
  • Histone Deacetylases