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Role of NF-B in TNF--induced COX-2 Expression in Synovial Fibroblasts from Human TMJ

¹ Key Lab. for Oral Biomedical Engineering, Ministry of Education,
² Departments of Oral Maxillofacial Surgery and
⁴ Prosthodontics, School & Hospital of Stomatology,
³ Department of Radio-Chemotherapy of Zhongnan Hospital, Wuhan University, Wuhan 430079, PR China

^* corresponding author, longxing_china{at}hotmail.com

In the temporomandibular joint (TMJ) synovium, cyclo-oxygenase-2 (COX-2) expression has been believed to be directly related to joint pain and synovitis. Here we investigated the role of Nuclear Factor B (NF-B) in the regulation of COX-2 expression in synovial fibroblasts from human TMJ induced by tumor necrosis factor- (TNF-). By reverse-transcriptase/polymerase chain-reaction (RT-PCR) and Western blotting analysis, TNF- induced a dose- and time-dependent increase in COX-2 expression. Electrophoretic mobility shift assay (EMSA) revealed that transient NF-B activation in the COX-2 promoter was triggered by TNF-. In parallel with transient NF-B activation, the rapid translocation of NF-B, particularly the p65 subunit, from the cytoplasm into the nucleus was demonstrated. Pre-treatment with pyrolidine dithiocarbamate (PDTC), one of the NF-B inhibitors, prevented binding to the COX-2 promoter and expression of COX-2 protein in response to TNF-. These findings indicate that activation of NF-B is responsible for TNF--induced COX-2 expression in synovial fibroblasts from the TMJ.

KEY WORDS: TMJ • COX-2 • NF-B • TNF- • synovial fibroblasts