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Inhibition by dexamethasone of interleukin 13 production via glucocorticoid receptor‐mediated inhibition of c‐Jun phosphorylation
Author(s) -
Hirasawa Noriyasu,
Izumi Shinichiroh,
Linwong Watchara,
Ohuchi Kazuo
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)01228-6
Subject(s) - phosphorylation , c jun , glucocorticoid receptor , glucocorticoid , dexamethasone , chemistry , stimulation , kinase , microbiology and biotechnology , endocrinology , medicine , pharmacology , biology , biochemistry , gene , transcription factor
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.