The effects of static and intermittent compression on nitric oxide production in articular cartilage explants
Nitric oxide (NO) production and NO synthase (NOS) expression are increased in osteoarthritis and rheumatoid arthritis, suggesting that NO may play a role in the destruction of articular cartilage. To test the hypothesis that mechanical stress may increase NO production by chondrocytes, we measured...
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Published in | Journal of orthopaedic research Vol. 19; no. 4; pp. 729 - 737 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Hoboken
Elsevier Ltd
01.07.2001
Wiley Subscription Services, Inc., A Wiley Company Blackwell Publishing Ltd |
Subjects | |
Online Access | Get full text |
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Summary: | Nitric oxide (NO) production and NO synthase (NOS) expression are increased in osteoarthritis and rheumatoid arthritis, suggesting that NO may play a role in the destruction of articular cartilage. To test the hypothesis that mechanical stress may increase NO production by chondrocytes, we measured the effects of physiological levels of static and intermittent compression on NOS activity, NO production, and NOS antigen expression by porcine articular cartilage explants. Static compression significantly increased NO production at 0.1 MPa stress for 24 h (
P<0.05). Intermittent compression at 0.5 Hz for 6 h followed by 18 h recovery also increased NO production and NOS activity at 1.0 MPa stress (
P<0.05). Intermittent compression at 0.5 Hz for 24 h at a magnitude of 0.1 or 0.5 MPa caused an increase in NO production and NOS activity (
P<0.05). Immunoblot analysis showed stress-induced upregulation of NOS2, but not NOS1 or NOS3. There was no loss in cell viability following any of the loading regimens. Addition of 2 mM 1400 W (a specific NOS2 inhibitor) reduced NO production by 51% with no loss of cell viability. These findings indicate that NO production by chondrocytes is influenced by mechanical compression in vitro and suggest that biomechanical factors may in part regulate NO production in vivo. |
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Bibliography: | ark:/67375/WNG-NV41GL24-N Flexcell International, Inc. istex:F2CA8780A6E401A052C66DF833F938CD56523DEE ArticleID:JOR1100190434 NIH - No. AR39162; No. AR43876; No. AG15768 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0736-0266 1554-527X |
DOI: | 10.1016/S0736-0266(00)00049-8 |