Hydrogen peroxide activation of ERK5 confers resistance to Jurkat cells against apoptosis induced by the extrinsic pathway

Takeshi Suzuki, Jay Yang

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Reactive oxygen species (ROS) including hydrogen peroxide (H 2O2) exhibit both pro-survival and pro-death signaling in leukemic cells. We examined the effect of exogenous H2O2 on Fas ligand (FasL) -induced apoptosis in Jurkat cells. H2O 2 applied prior to (pre-conditioning) and during (post-conditioning) FasL stimulation attenuated early apoptosis through activation of EKR5. H 2O2 increased the activated caspase-8 sequestered in the mitochondria thereby decreasing cell death through the extrinsic apoptotic pathway. In addition, inhibition of a protein tyrosine phosphatase likely explains the post-conditioning requirement for H2O2. Given that chemotherapeutic agents used for the treatment of acute lymphoblastic leukemia are thought to work partly through production of ROS, a simultaneous inhibition of the ERK5 pathway may abrogate the ROS-initiated pro-survival signaling for an enhanced cell kill.

Original languageEnglish
Pages (from-to)248-253
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume444
Issue number2
DOIs
Publication statusPublished - 2014 Feb 7

Fingerprint

Jurkat Cells
Hydrogen Peroxide
Reactive Oxygen Species
Fas Ligand Protein
Chemical activation
Apoptosis
Mitochondria
Protein Tyrosine Phosphatases
Caspase 8
Cell death
Precursor Cell Lymphoblastic Leukemia-Lymphoma
Cell Death

Keywords

  • Apoptosis
  • Extrinsic pathway
  • FAS ligand
  • Hydrogen peroxide
  • Jurkat cell

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Molecular Biology

Cite this

Hydrogen peroxide activation of ERK5 confers resistance to Jurkat cells against apoptosis induced by the extrinsic pathway. / Suzuki, Takeshi; Yang, Jay.

In: Biochemical and Biophysical Research Communications, Vol. 444, No. 2, 07.02.2014, p. 248-253.

Research output: Contribution to journalArticle

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