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Nitric oxide synthesis of bovine articular chondrocytes induced by thrombin not through the thrombin receptor, protease-activated receptor-1 (PAR-1)

Bulletin of health sciences Kobe

18

23-30

Graduate School of Health Sciences, Kobe University

2002-12-20

2006-09-11

本文ファイルは、国立情報学研究所CiNiiより提供されたものです。

High level of thrombin-antithrombin III complex is detected in the synovial fluid of rheumatoid arthritis (RA) patients, and thrombin induces the release of proteoglycans from articular cartilage and stimulates proliferation of synovial fibroblasts. These findings suggest that thrombin plays an important role in propagation of inflammation and cartilage degradation in RA. Nitric oxide (NO) is reported to reduce the synthesis of matrix components by chondrocytes, which should cause the deterioration of functional property of the articular cartilage. Therefore, we studied the NO synthesis of articular chondrocytes by thrombin in order to examine the role of thrombin for evidence of cartilage degradation in inflammatory process. When cells were cultured with thrombin for 48 hours, promotion of NO generation was observed in a dose dependent fashion. 100 μM of pyrolidine dithiocarbamate (PDTC), an inhibitor of nuclear factor kappa B (NF-kB) completely inhibited NO release. However, thrombin receptor agonist specific for protease-activated receptor-1 (PAR-1) had little effect on NO release of chondrocytes. These results suggested that thrombin regulated NO synthesis by NF-kB activation through a PAR-1 independent pathway in chondrocytes.

Protease-activated receptor-1

紀要論文