Regulation of lubricin gene expression and synthesis in cartilage by mechanical injury

Articular cartilage is the connective tissue which lines the bony ends of diathrodial joints to provide load distribution and frictionless motion. Lubricin, a glycoprotein which concentrates at the superficial layer of the cartilage, contributes to the low friction coefficient. Mechanical injury to cartilage increases the risk of osteoarthritis (OA), characterized by degradation of articular cartilage starting with the articular surface. The objectives of this study were to quantify the effects of injurious compression on the surface mechanical properties of cartilage, and lubricin gene expression and synthesis using an in vitro organ culture model. Furthermore, the role of TGF-P signaling in the induction of lubricin gene expression and protein secretion from cartilage explants following mechanical injury was analyzed. Cartilage disks with intact superficial zone from the patellofemoral grooves of 1-2 wk old bovine knees were cultured in either free swelling conditions or subjected to injurious compression using a range of applied strains and strain rates. Mechanical injury was found to elevate the friction coefficient of cartilage. Average surface roughness of cartilage superficial zone was increased by the combination of injury and subsequent oscillating shear motion at the surface superimposed on an applied normal strain. RNA extraction and qRT-PCR were conducted sequentially to determine the expression of lubricin and other relevant cartilage genes. Western blotting and ELISA were used to assess protein expression. Lubricin gene expression and secretion increased two days after injury.

Department dc:contributor.department

Massachusetts Institute of Technology. Dept. of Electrical Engineering and Computer Science.

Grantor dc:publisher

Massachusetts Institute of Technology

Year dc:date.issued

2009

Author dc:creator

• Chen, Shuodan

Advisor dc:contributor.advisor

• Alan J. Grodzinsky.

• Electrical Engineering and Computer Science.

Statement dc:rights

• M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission.

Licence dc:rights.uri

• http://dspace.mit.edu/handle/1721.1/7582

Language dc:language.iso

eng

Handle dc:identifier.uri

http://hdl.handle.net/1721.1/55094

OAI identifier oai:identifier

oai:dspace.mit.edu:1721.1/55094