Inhibition by dexamethasone of interleukin 13 production via glucocorticoid receptor‐mediated inhibition of c‐Jun phosphorylation

FEBS Letters

Linwong, Watchara¹  Ohuchi, Kazuo¹  Hirasawa, Noriyasu¹  Izumi, Shinichiroh¹ 

[1] Laboratory of Pathophysiological Biochemistry, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba Aramaki, Aoba-ku, Sendai, Miyagi 980-8578, Japan

关键词: Dexamethasone;    c-Jun N-terminal kinase;    c-Jun;    Glucocorticoid receptor;    Interleukin 13;    RBL-2H3 cell line;    AP-1;    activating protein 1;    BSA;    bovine serum albumin;    CBP;    CREB binding protein;    DMSO;    dimethylsulfoxide;    DNP;    dinitrophenyl;    EMEM;    Eagle's minimal essential medium;    FBS;    fetal bovine serum;    GR;    glucocorticoid receptor;    GST;    glutathione S-transferase;    HSA;    human serum albumin;    IL-13;    interleukin 13;    JNK;    c-Jun N-terminal kinase;    MAP;    mitogen-activated protein;    MEK;    MAP extracellular signal regulated kinase kinase;   

DOI  :  10.1016/S0014-5793(03)01228-6

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The antigen stimulation of RBL-2H3 cells induced interleukin 13 (IL-13) production, which was inhibited by the steroidal anti-inflammatory drug dexamethasone and by the c-Jun N-terminal kinase (JNK) inhibitor SP600125. Dexamethasone did not inhibit the antigen-induced phosphorylation of JNK but inhibited that of c-Jun. In a cell-free system, the phosphorylation of glutathione S-transferase-fused c-Jun by recombinant JNK was not inhibited by dexamethasone but was inhibited by the addition of recombinant glucocorticoid receptor (GR). These findings suggest that the inhibition of antigen-induced IL-13 production by dexamethasone is due to the GR-mediated inhibition of c-Jun phosphorylation induced by JNK.

【 授权许可】

Unknown