title: Alteration of articular cartilage frictional properties by transforming growth factor beta, interleukin-1beta, and oncostatin M.
abstract: OBJECTIVE
  To evaluate the functional effects of transforming growth factor beta1 (TGFbeta1), interleukin-1beta (IL-1beta), and oncostatin M (OSM) on the frictional properties of articular cartilage and to determine the role of cytokine-mediated changes in cartilage frictional properties by extracting and redepositing lubricin on the surface of cartilage explants.
  
  
  METHODS
  Neonatal bovine cartilage explants were cultured in the presence or absence of 10 ng/ml of TGFbeta1, IL-1beta, or OSM over 48 hours. Boundary lubrication tests were conducted to determine the effects of endogenously produced surface localized lubricin and of exogenous lubricin at the tissue surface and in the lubricant solution. The initial friction coefficient (micro(0)), equilibrium friction coefficient (micro(eq)), and Young's modulus (E(Y)) were determined from the temporal load data.
  
  
  RESULTS
  IL-1beta and OSM decreased tissue glycosaminoglycan (GAG) content by approximately 20% over 48 hours and decreased E(Y) to a similar extent (11-17%), but TGFbeta did not alter GAG content or E(Y). Alterations in proteoglycan content corresponded to changes in micro(0), but endogenous lubricin decreased boundary mode micro(eq). The addition of exogenous lubricin, either localized at the tissue surface or in the lubricating solution, did not modulate micro(0), but it did lower micro(eq) in cytokine-treated cartilage.
  
  
  CONCLUSIONS
  This study provides new insight into the functional consequences of cytokine-mediated changes in friction coefficient. In combination with established pathways of cytokine-mediated lubricin metabolism, these data provide evidence of distinct biochemical origins of boundary and biphasic pressure-mediated lubrication mechanisms in cartilage, with boundary lubrication regulated by surface accumulation of lubricants and biphasic lubrication controlled by factors such as GAG content that affect water movement through the tissue.
authors.affiliation: Cornell University, Ithaca, New York, USA.
authors.forename: Jason P
authors.initials: JP
authors.lastname: Gleghorn
authors.forename: Aled R C
authors.initials: AR
authors.lastname: Jones
authors.forename: Carl R
authors.initials: CR
authors.lastname: Flannery
authors.forename: Lawrence J
authors.initials: LJ
authors.lastname: Bonassar
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002358:Cartilage, Articular / Q000737:chemistry / Q000187:drug effects* / Q000378:metabolism; D002417:Cattle; D017276:Friction; D006023:Glycoproteins / Q000378:metabolism; D006025:Glycosaminoglycans / Q000032:analysis / Q000378:metabolism; D006131:Growth Inhibitors / Q000494:pharmacology*; D053583:Interleukin-1beta / Q000494:pharmacology*; D008153:Lubrication; D053683:Oncostatin M / Q000494:pharmacology*; D013499:Surface Properties; D013582:Synovial Fluid / Q000187:drug effects / Q000378:metabolism; D046509:Tissue Culture Techniques; D016212:Transforming Growth Factor beta / Q000494:pharmacology*; D000099158:Proteoglycan 4
chemical_list: D006023:Glycoproteins; D006025:Glycosaminoglycans; D006131:Growth Inhibitors; D053583:Interleukin-1beta; D053683:Oncostatin M; D016212:Transforming Growth Factor beta; D000099158:Proteoglycan 4