Tanaka Tomoko, Okabe Taijiro, Gondo Shigeki, Fukuda Mitsue, Yamamoto Masahiro, Umemura Tsukuru, Tani Kenzaburo, Nomura Masatoshi, Goto Kiminobu, Yanase Toshihiko, Nawata Hajime
Department of Medicine and Bioregulatory Science, Graduate School of Medical Science, Kyushu University, Fukuoka, Japan.
Exp Hematol. 2006 Nov;34(11):1542-52. doi: 10.1016/j.exphem.2006.06.018.
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.
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.
These findings might provide new tools for overcoming glucocorticoid-resistance.
糖皮质激素广泛用于治疗血液系统恶性肿瘤等疾病。糖皮质激素敏感性因人而异，其敏感性调节机制尚不明确。糖皮质激素抵抗是一个主要的临床问题。
在此，我们利用糖皮质激素诱导的T细胞凋亡这一用于分析糖皮质激素作用机制的模型系统，阐明了丝裂原活化蛋白激酶（MAPKs）可调节糖皮质激素敏感性，即细胞外信号调节蛋白激酶（ERK）的激活降低糖皮质激素敏感性，而p38 MAP激酶的激活则增强糖皮质激素敏感性。
这些发现可能为克服糖皮质激素抵抗提供新的手段。
