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BK‐induced COX‐2 expression via PKC‐δ‐dependent activation of p42/p44 MAPK and NF‐κB in astrocytes
Author(s) -
Hsieh HsiLung,
Yang ChuenMao
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a695-c
Subject(s) - rottlerin , mapk/erk pathway , protein kinase c , phosphorylation , microbiology and biotechnology , chemistry , biology
BK has been shown to induce COX‐2 expression response to inflammation in various cell types. However, the mechanisms underlying BK‐induced COX‐2 expression in astrocytes remain unclear. BK‐induced COX‐2 expression was inhibited by B 2 BK receptor antagonist (Hoe140), PKC inhibitor (rottlerin), and transfection with a dominant negative plasmid of PKC‐δ, suggesting that PKC‐δ might be involved in the response. BK‐stimulated p42/p44 MAPK phosphorylation, COX‐2 expression, and PGE 2 release were attenuated by PD98059, indicating the involvement of p42/p44 MAPK in these responses. BK‐stimulated phosphorylation of p42/p44 MAPK was attenuated by rottlerin, indicating that PKC‐δ might be an upstream component of p42/p44 MAPK. Moreover, BK‐induced COX‐2 expression might be due to the translocation of NF‐κB into nucleus which was blocked by helenalin, rottlerin and PD98059. These results suggest that in RBA‐1 cells, BK‐induced COX‐2 expression was sequentially mediated through PKC‐δ‐dependent activation of p42/p44 MAPK and NF‐κB.