Journal
JOURNAL OF ORAL PATHOLOGY & MEDICINE
Volume 38, Issue 7, Pages 584-590Publisher
WILEY
DOI: 10.1111/j.1600-0714.2008.00733.x
Keywords
COX-2; fibroblast-like synoviocytes; IL-1 beta; oligonucleotide microarray; synovitis; TMJ
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Funding
- Japan Society for the Promotion of Science [17592111, 19592318]
- Grants-in-Aid for Scientific Research [19592318, 17592111] Funding Source: KAKEN
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Background: In this study, we analyzed the gene expression profile of fibroblast-like synoviocyte (FLS) cultures from the temporomandibular joint (TMJ) to identify candidate genes associated with intracapsular pathologic conditions of TMJ. Cyclooxygenase (COX)-2 was one of the genes in FLS upregulated following stimulation by interleukin (IL)-1 beta, a cytokine thought to play a key role in several pathological conditions. This study investigated the expression of COX-1 and COX-2 in cultured human FLS and rat TMJ synovium following stimulation with IL-1 beta. Methods: RNA was isolated from human FLS after IL-1 beta treatment. COX-1 and -2 expression was examined using a GeneChip and real-time polymerase chain reaction. Prostaglandin E-2 (PGE(2)) levels in conditioned media from FLS were measured using enzyme-linked immunosorbent assay. Synovial tissues from TMJs of IL-1 beta-injected rats were examined for COX-1 and COX-2 expression by immunohistochemical staining. Results: Following treatment of FLS with IL-1 beta, expression of the COX-2 gene increased up to 8 h and peaked at 4 h, whereas COX-1 expression did not change. Stimulation with IL-1 beta increased the level of PGE(2) in conditioned media of cultured FLS in a time-dependent manner up to 48 h. Immunohistochemistry showed a strong positive staining for COX-2 in the lining and sub-lining synovial tissues of the TMJ of IL-1 beta-injected rats. In contrast, staining for COX-1 was the same in synovial tissues with and without IL-1 beta injection. Conclusion: These data suggest that COX-2 expression stimulated by IL-1 beta stimulates the production of PGE(2) in FLS and plays important roles in the progression of inflammation in TMJ.
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