Activation of c-Jun N-terminal kinase is essential for oxidative stress-induced Jurkat cell apoptosis by monochloramine

Tetsuya Ogino, Michitaka Ozaki, Mutsumi Hosako, Masako Omori, Shigeru Okada, Akihiro Matsukawa

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Leukemic cell apoptosis may be enhanced by appropriate oxidative stress. We report here the mechanism of Jurkat cell apoptosis by monochloramine (NH2Cl), a neutrophil-derived oxidant. NH2Cl induced caspase-dependent apoptosis, which was preceded by cytochrome c and Smac/Diablo release from mitochondria. Within 10 min of NH2Cl treatment, c-Jun N-terminal kinase (JNK) activation and elevation of cytosolic Ca2+ were observed. JNK inhibitors (SP600125 or JNK inhibitor VIII) significantly suppressed the apoptosis as well as caspase cleavage and cytochrome c release. In contrast, Ca2+ chelation by EGTA + acetoxymethyl-EGTA had no effects on apoptosis. Our results indicated that JNK activation contributed most importantly to the NH2Cl-induced apoptosis.

Original languageEnglish
Pages (from-to)151-158
Number of pages8
JournalLeukemia Research
Volume33
Issue number1
DOIs
Publication statusPublished - Jan 2009

Keywords

  • Apoptosis
  • Calcium
  • Chemotherapy
  • Mitochondria
  • Oxidative stress
  • c-Jun N-terminal kinase

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research

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