Modulation of lubricin biosynthesis and tissue surface properties following cartilage mechanical injury
Shuodan Chen
Massachusetts Institute of Technology, Cambridge, Massachusetts
Search for more papers by this authorDiana H. Chai
Massachusetts Institute of Technology, Cambridge, Massachusetts
Search for more papers by this authorAnna L. Stevens
Massachusetts Institute of Technology, Cambridge, Massachusetts
Search for more papers by this authorAlan J. Grodzinsky
Massachusetts Institute of Technology, Cambridge, Massachusetts
Search for more papers by this authorCorresponding Author
Carl R. Flannery
Wyeth Research, Cambridge, Massachusetts
Dr. Flannery owns stock or stock options in Wyeth.
Wyeth Research, 200 Cambridge Park Drive, Cambridge, MA 02140Search for more papers by this authorShuodan Chen
Massachusetts Institute of Technology, Cambridge, Massachusetts
Search for more papers by this authorDiana H. Chai
Massachusetts Institute of Technology, Cambridge, Massachusetts
Search for more papers by this authorAnna L. Stevens
Massachusetts Institute of Technology, Cambridge, Massachusetts
Search for more papers by this authorAlan J. Grodzinsky
Massachusetts Institute of Technology, Cambridge, Massachusetts
Search for more papers by this authorCorresponding Author
Carl R. Flannery
Wyeth Research, Cambridge, Massachusetts
Dr. Flannery owns stock or stock options in Wyeth.
Wyeth Research, 200 Cambridge Park Drive, Cambridge, MA 02140Search for more papers by this authorAbstract
Objective
To evaluate the effects of injurious compression on the biosynthesis of lubricin at different depths within articular cartilage and to examine alterations in structure and function of the articular surface following mechanical injury.
Methods
Bovine cartilage explants were subdivided into level 1, with intact articular surface, and level 2, containing middle and deep zone cartilage. Following mechanical injury, lubricin messenger RNA (mRNA) levels were monitored by quantitative reverse transcriptase–polymerase chain reaction, and soluble or cartilage-associated lubricin protein was analyzed by Western blotting and immunohistochemistry. Cartilage morphology was assessed by histologic staining, and tissue functionality was assessed by friction testing.
Results
Two days after injury, lubricin mRNA expression was up-regulated ∼3-fold for level 1 explants and was down-regulated for level 2 explants. Lubricin expression in level 1 cartilage returned to control levels after 6 days in culture. Similarly, lubricin protein synthesis and secretion increased in response to injury for level 1 explants and decreased for level 2 cartilage. Histologic staining revealed changes in the articular surface of level 1 explants following injury, with respect to glycosaminoglycan and collagen content. Injured level 1 explants displayed an increased coefficient of friction relative to controls.
Conclusion
Our findings indicate that increased lubricin biosynthesis appears to be an early transient response of surface-layer cartilage to injurious compression. However, distinct morphologic changes occur with injury that appear to compromise the frictional properties of the tissue.
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