Modification of glucocorticoid sensitivity by MAP kinase signaling pathways in glucocorticoid-induced T-cell apoptosis

Tomoko Tanaka; Taijiro Okabe; Shigeki Gondo; Mitsue Fukuda; Masahiro Yamamoto; Tsukuru Umemura; Kenzaburo Tani; Masatoshi Nomura; Kiminobu Goto; Toshihiko Yanase; Hajime Nawata

doi:10.1016/j.exphem.2006.06.018

Modification of glucocorticoid sensitivity by MAP kinase signaling pathways in glucocorticoid-induced T-cell apoptosis

Tomoko Tanaka, Taijiro Okabe, Shigeki Gondo, Mitsue Fukuda, Masahiro Yamamoto, Tsukuru Umemura, Kenzaburo Tani, Masatoshi Nomura, Kiminobu Goto, Toshihiko Yanase, Hajime Nawata

Department of Endocrine and Metabolic Diseases / Diabetes Mellitus

Research output: Contribution to journal › Article › peer-review

19 Citations (Scopus)

Abstract

Objective: Glucocorticoid is widely used for the treatment of diseases such as hematological malignancies. Glucocorticoid sensitivity is different from person to person and the mechanism of the regulation of glucocorticoid sensitivity is not well known. Glucocorticoid resistance is a major clinical problem. Methods and Results: Here, using glucocorticoid-induced T-cell apoptosis, a model system for the analysis of the mechanism of glucocorticoid action, we clarified that mitogen-activated protein kinases (MAPKs) modify glucocorticoid sensitivity, namely that the activation of extracellular signal-regulated protein kinase (ERK) and p38 MAP kinase reduce and enhance glucocorticoid sensitivity, respectively. Conclusion: These findings might provide new tools for overcoming glucocorticoid-resistance.

Original language	English
Pages (from-to)	1542-1552
Number of pages	11
Journal	Experimental Hematology
Volume	34
Issue number	11
DOIs	https://doi.org/10.1016/j.exphem.2006.06.018
Publication status	Published - Nov 2006

All Science Journal Classification (ASJC) codes

Molecular Biology
Hematology
Genetics
Cell Biology
Cancer Research

UN SDGs

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

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10.1016/j.exphem.2006.06.018

Cite this

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title = "Modification of glucocorticoid sensitivity by MAP kinase signaling pathways in glucocorticoid-induced T-cell apoptosis",

abstract = "Objective: Glucocorticoid is widely used for the treatment of diseases such as hematological malignancies. Glucocorticoid sensitivity is different from person to person and the mechanism of the regulation of glucocorticoid sensitivity is not well known. Glucocorticoid resistance is a major clinical problem. Methods and Results: Here, using glucocorticoid-induced T-cell apoptosis, a model system for the analysis of the mechanism of glucocorticoid action, we clarified that mitogen-activated protein kinases (MAPKs) modify glucocorticoid sensitivity, namely that the activation of extracellular signal-regulated protein kinase (ERK) and p38 MAP kinase reduce and enhance glucocorticoid sensitivity, respectively. Conclusion: These findings might provide new tools for overcoming glucocorticoid-resistance.",

author = "Tomoko Tanaka and Taijiro Okabe and Shigeki Gondo and Mitsue Fukuda and Masahiro Yamamoto and Tsukuru Umemura and Kenzaburo Tani and Masatoshi Nomura and Kiminobu Goto and Toshihiko Yanase and Hajime Nawata",

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T1 - Modification of glucocorticoid sensitivity by MAP kinase signaling pathways in glucocorticoid-induced T-cell apoptosis

AU - Tanaka, Tomoko

AU - Okabe, Taijiro

AU - Gondo, Shigeki

AU - Fukuda, Mitsue

AU - Yamamoto, Masahiro

AU - Umemura, Tsukuru

AU - Tani, Kenzaburo

AU - Nomura, Masatoshi

AU - Goto, Kiminobu

AU - Yanase, Toshihiko

AU - Nawata, Hajime

PY - 2006/11

Y1 - 2006/11

N2 - Objective: Glucocorticoid is widely used for the treatment of diseases such as hematological malignancies. Glucocorticoid sensitivity is different from person to person and the mechanism of the regulation of glucocorticoid sensitivity is not well known. Glucocorticoid resistance is a major clinical problem. Methods and Results: Here, using glucocorticoid-induced T-cell apoptosis, a model system for the analysis of the mechanism of glucocorticoid action, we clarified that mitogen-activated protein kinases (MAPKs) modify glucocorticoid sensitivity, namely that the activation of extracellular signal-regulated protein kinase (ERK) and p38 MAP kinase reduce and enhance glucocorticoid sensitivity, respectively. Conclusion: These findings might provide new tools for overcoming glucocorticoid-resistance.

AB - Objective: Glucocorticoid is widely used for the treatment of diseases such as hematological malignancies. Glucocorticoid sensitivity is different from person to person and the mechanism of the regulation of glucocorticoid sensitivity is not well known. Glucocorticoid resistance is a major clinical problem. Methods and Results: Here, using glucocorticoid-induced T-cell apoptosis, a model system for the analysis of the mechanism of glucocorticoid action, we clarified that mitogen-activated protein kinases (MAPKs) modify glucocorticoid sensitivity, namely that the activation of extracellular signal-regulated protein kinase (ERK) and p38 MAP kinase reduce and enhance glucocorticoid sensitivity, respectively. Conclusion: These findings might provide new tools for overcoming glucocorticoid-resistance.

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Modification of glucocorticoid sensitivity by MAP kinase signaling pathways in glucocorticoid-induced T-cell apoptosis

Abstract

All Science Journal Classification (ASJC) codes

UN SDGs

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