Affiliations: Department of Pathology, University of Bristol Medical School, Bristol BS8 1TD, UK | Department of Physiology, University of Oxford, Oxford OX1 3PT, UK | Harvard Medical School Division of Rheumatology, Beth Israel Deaconess Medical Centre, Boston, MA, USA
Note: [] Address for correspondence: Carole I. Westacott, PhD, Department of Pathology and Microbiology, School of Medical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, UK. Tel.: +44 117 9288605; Fax: +44 117 9287896; E‐mail: Carole.Westacott@bristol.ac.uk.
Abstract: This work was performed to determine whether one aspect of load, pressure, could alter tumour necrosis factor (TNF) receptor type I (RI) expression on chondrocytes. Encapsulated tsT/AC62, osteoarthritic (OA) or non‐arthritic (NA) chondrocytes were centrifuged at speeds representing 5 or 20 MPa, incubated for specific periods, released from alginate and TNFRI and II (TNFRII) expression determined by flow cytometry. Significant (p<0.05, n=4) changes in tsT/AC62 chondrocyte TNFRI expression were apparent 24 hours after application of 20 MPa. Five or 20 MPa increased OA chondrocyte TNFRI expression; chondrocytes from some OA patients were markedly sensitive to 20 MPa. NA chondrocyte TNFRI expression usually decreased in response to 5 and 20 MPa. Significant pressure‐induced differences in TNFRI expression between NA and OA groups were apparent at 5, but not 20 MPa. Pressure did not significantly alter TNRFII expression on tsT/AC62, NA or OA chondrocytes. These results suggest a mechanism whereby sensitivity of chondrocytes to the effects of TNFα may be increased, in susceptible individuals, in regions of the joint that experience peak loading.
Journal: Biorheology, vol. 39, no. 1-2, pp. 125-132, 2002
