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Involvement of MAPKs and NF‐κB in cPLA 2 induced by IL‐1β in tracheal smooth muscle cells
Author(s) -
Chen HsinChieh,
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.20.5.a1444
Subject(s) - wortmannin , staurosporine , protein kinase c , ly294002 , microbiology and biotechnology , iκb kinase , signal transduction , tyrosine kinase , kinase , nf κb , chemistry , stimulation , protein kinase b , endocrinology , biology
cPLA 2 plays a pivotal role in mediating agonist‐induced AA release for PG synthesis during stimulation with IL‐1β. However, the signaling pathways mediating cPLA 2 expression and PGE 2 synthesis by canine tracheal smooth muscle cells (TSMCs) remain unknown. IL‐1β‐induced cPLA 2 expression and PGE 2 release were attenuated by inhibitors of tyrosine kinase (genistein), PC‐PLC (D609), PI‐PLC (U73122), PKC (GF109203X and staurosporine), Ca 2+ (BAPTA+EDTA), MEK1/2 (PD98059), p38 (SB202190), JNK (SP600125), and PI3‐K (LY294002 and wortmannin). In addition, IL‐1β‐induced cPLA 2 expression and PGE 2 synthesis was attenuated by transfection with dominant negative mutants of NF‐κB inducing kinase (NIK) and IκB kinase (IKK)‐α, but not by IKK‐β. Taken together, these findings suggest that the increased expression of cPLA 2 correlates with the release of PGE 2 from IL‐1β‐challenged TSMCs, at least in part, mediated through MAPKs and NF‐κB signaling pathways. IL‐1β‐mediated responses were modulated by PLC, Ca 2+ , PKC, tyrosine kinase, and PI3‐K in these cells.