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

doi:10.1016/j.leukres.2008.07.009

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 journal › Article › peer-review

15 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 language	English
Pages (from-to)	151-158
Number of pages	8
Journal	Leukemia Research
Volume	33
Issue number	1
DOIs	https://doi.org/10.1016/j.leukres.2008.07.009
Publication status	Published - Jan 2009

Keywords

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

ASJC Scopus subject areas

Hematology
Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.leukres.2008.07.009

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

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.",

keywords = "Apoptosis, Calcium, Chemotherapy, Mitochondria, Oxidative stress, c-Jun N-terminal kinase",

author = "Tetsuya Ogino and Michitaka Ozaki and Mutsumi Hosako and Masako Omori and Shigeru Okada and Akihiro Matsukawa",

note = "Funding Information: MH is a recipient of a grant from the Japan Leukemia Research Fund. Funding Information: This study was supported by the Program for Promotion of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovation (NIBIO).",

year = "2009",

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doi = "10.1016/j.leukres.2008.07.009",

language = "English",

volume = "33",

pages = "151--158",

journal = "Leukemia Research",

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T1 - Activation of c-Jun N-terminal kinase is essential for oxidative stress-induced Jurkat cell apoptosis by monochloramine

AU - Ogino, Tetsuya

AU - Ozaki, Michitaka

AU - Hosako, Mutsumi

AU - Omori, Masako

AU - Okada, Shigeru

AU - Matsukawa, Akihiro

N1 - Funding Information: MH is a recipient of a grant from the Japan Leukemia Research Fund. Funding Information: This study was supported by the Program for Promotion of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovation (NIBIO).

PY - 2009/1

Y1 - 2009/1

N2 - 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.

AB - 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.

KW - Apoptosis

KW - Calcium

KW - Chemotherapy

KW - Mitochondria

KW - Oxidative stress

KW - c-Jun N-terminal kinase

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DO - 10.1016/j.leukres.2008.07.009

M3 - Article

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SN - 0145-2126

VL - 33

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EP - 158

JO - Leukemia Research

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IS - 1

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

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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