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. This finding, plus the fact that injury and TGF-f are each known to increase lubricin expression, suggested that the TGF-3 signaling pathway may be a mechanism through which injury induces lubricin expression. We therefore tested the hypothesis that blocking the TGF-P pathway would suppress the increase in lubricin gene expression and protein secretion caused by injurious compression of cartilage. Indeed, lubricin gene expression and protein secretion were reduced after blocking TGF-f compared to injury alone. Together, these results show that surface damage caused injury and sliding motion can be ameliorated by the presence of lubricin on the cartilage surface. The TGF-3 pathway is an important mechanism in regulating the increased lubricin gene expression and secretion that result from injury.