Address: Department of Biomedical Engineering and Sibley School of Mechanical and Aerospace Engineering, 218 Upson Hall, Cornell University, Ithaca, NY 14853, USA

E-mail: LB244@cornell.edu

Key Words: friction, lubricin, PRG4, boundary lubrication, tissue engineering, chondrocytes, meniscal fibrochondrocytes, mesenchymal stem cells

Publication date: August 4th 2007

Abstract: Despite the fact that lubrication is a primary function of articular cartilage, there is little information on the frictional properties of cartilaginous engineered tissues. A biochemical mediator of cartilage frictional properties in boundary lubrication, lubricin, has been shown to be secreted from chondrocyte-hydrogel constructs. In the current studies we utilized articular chondrocytes (CON), meniscal fibrochondrocytes (MEN), and mesenchymal stem cells (MSC) in alginate cultures to determine lubricin localization and the inherent boundary lubrication friction coefficient. Additionally, we investigated the ability of these tissues to be lubricated by synovial fluid and the reversibility of this lubrication. Cell-alginate constructs were cultured over six weeks, culture medium assayed for lubricin release by ELISA and constructs analyzed with immunohistochemical (IHC) methods to investigate the localization of lubricin. Engineered tissues were tested in a custom friction instrument to determine the equilibrium friction coefficient (µeq) in boundary lubrication mode, following incubation with equine synovial fluid (SF), and subsequent extraction in l.5M NaCl. MSCs released 10 fold more lubricin than CON or MEN cultures. IHC analysis showed no localization of lubricin to alginate, minimal focal staining of engineered constructs at six weeks in culture, and the ability of all engineered tissues to localize lubricin when exogenously treated with SF. Frictional characterization showed no difference in µeq over culture for all engineered tissues, while incubation in SF decreased µeq for all tissues over culture duration, and extraction of lubricin resulted in a loss of lubrication of all engineered tissues.

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