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IL‐1β‐dependent activation of NF‐κB mediates PGE 2 release via the expression of cyclooxygenase‐2 and microsomal prostaglandin E synthase
Author(s) -
Catley Matthew C.,
Chivers Joanna E.,
Cambridge Lisa M.,
Holden Neil,
Slater Donna M.,
Staples Karl J.,
Bergmann Martin W.,
Loser Peter,
Barnes Peter J.,
Newton Robert
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)00672-0
Subject(s) - cyclooxygenase , atp synthase , chemistry , microsome , prostaglandin , microbiology and biotechnology , prostaglandin e , prostaglandin e2 , enzyme , biochemistry , endocrinology , biology
Prostaglandin (PG) E 2 release is induced in pulmonary A549 cells by the NF‐κB‐activating stimuli interleukin‐1β (IL‐1β) and phorbol 12‐myristate 13‐acetate (PMA). Adenoviral over‐expression of IκBαΔN, a dominant NF‐κB inhibitor, prevents NF‐κB‐dependent transcription and was used to qualify the role of NF‐κB in the release of PGE 2 . IκBαΔN repressed IL‐1β‐induced, but not PMA‐induced, cycloxygenase‐2 (COX‐2) and microsomal prostaglandin E synthase (mPGES) expression. These data conclusively demonstrate a substantial role for NF‐κB in the co‐ordinate induction of COX‐2, mPGES and in the corresponding release of PGE 2 by IL‐1β. However, other pathways are primarily responsible for PGE 2 release induced by PMA.