Modification of glucocorticoid sensitivity by MAP kinase signaling pathways in glucocorticoid-induced T-cell apoptosis
Modification of glucocorticoid sensitivity by MAP kinase signaling pathways in glucocorticoid-induced T-cell apoptosis
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DOI：
10.1016/j.exphem.2006.06.018
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发表时间：
2006-11-01
影响因子：
2.6
通讯作者：
Nawata, Hajime
中科院分区：
文献类型：
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作者：
Tanaka, Tomoko;Okabe, Taijiro;Nawata, Hajime
Objective.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，其调节机制尚不清楚。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细胞凋亡模型系统分析糖皮质激素的作用机制，阐明丝裂原活化蛋白激酶（MAPK）改变糖皮质激素的敏感性，即细胞外信号调节蛋白激酶（ERK）和p38 MAP激酶的激活分别降低和增强糖皮质激素的敏感性。这些发现可能为克服糖皮质激素抵抗提供新的工具。(c)2006年国际实验血液学学会。爱思唯尔公司出版
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. (c) 2006 International Society for Experimental Hematology. Published by Elsevier Inc.