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

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18 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 languageEnglish
Pages (from-to)1542-1552
Number of pages11
JournalExperimental Hematology
Volume34
Issue number11
DOIs
Publication statusPublished - Nov 2006

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Hematology
  • Genetics
  • Cell Biology
  • Cancer Research

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    Tanaka, T., Okabe, T., Gondo, S., Fukuda, M., Yamamoto, M., Umemura, T., Tani, K., Nomura, M., Goto, K., Yanase, T., & Nawata, H. (2006). Modification of glucocorticoid sensitivity by MAP kinase signaling pathways in glucocorticoid-induced T-cell apoptosis. Experimental Hematology, 34(11), 1542-1552. https://doi.org/10.1016/j.exphem.2006.06.018