期刊
CONNECTIVE TISSUE RESEARCH
卷 50, 期 3, 页码 186-193出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/03008200802588451
关键词
Chondrocytes; PGE2; IL-1; PG Receptors; Cyclooxygenase
资金
- Japanese Society for the Promotion of Science [19592182, 19791384]
- Nihon University Multidisciplinary Research Grant [2006-2007]
- Nihon University Research Grant for Assistants and Young Researchers [2007]
- Promotion and Mutual Aid Corporation for Private Schools of Japan
- Sato Fund of Nihon University School of Dentistry
Prostaglandin (PG) E2, which exerts its actions via the PG receptors EP1-4, is produced from arachidonic acid by cyclooxygenase (COX)-1 and COX-2. The aim of this study was to investigate the mechanisms by which interleukin (IL)-1 induces the expression of PG receptors in cultured human chondrocytes and to explore the role of PGE2 in this process. The cells were cultured with 0, 10, or 100 U/mL IL-1 with or without 1 M celecoxib, a specific inhibitor of COX-2, for up to 28 days. Expression of the genes encoding COX-1, COX-2, and EP1-4 was quantified using real-time PCR, and expression of the corresponding proteins was examined using immunohistochemical staining. PGE2 production was determined using ELISA. IL-1 treatment caused a marked dose- and time-dependent increase in the levels of PGE2, COX-2, and EP4 as compared with the untreated control. It did not affect the expression of COX-1, and it decreased the expression of EP1 and EP2. EP3 expression was not detected in either the absence or the presence of IL-1. When celecoxib was also present, IL-1 failed to stimulate PGE2 production and EP4 expression, but its stimulatory effect on COX-2 expression and its inhibitory effect on EP1 and EP2 expression were unchanged. IL-1 increases the production of PGE2, COX-2, and the PG receptor EP4 in cultured human chondrocytes. The increase in EP4 expression appears to be a result of the increased PGE2 production.
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