Vitronectin expression in rheumatoid arthritic synovia - Inhibition of plasmin generation by vitronectin produced in vitro

Abstract

The plasmin-generating system controls, to a great extent, the degree of connective tissue destruction as well as fibrin deposition-two contributors to the pathogenesis generated in diseases such as rheumatoid arthritis. Vitronectin, an adhesive blood glycoprotein, has the potential to modulate this system by its known capacity to interact with plasminogen activator inhibitor-1, plasminogen activators, the urokinase plasminogen activator receptor, and plasminogen. The net effect of these interactions, in terms of plasmin generation, is not known as yet. In the present study, we have investigated the possible expression and role of vitronectin in rheumatoid arthritic synovia. Analysis of synovial frozen sections by immunofluorescence showed the presence of vitronectin in the 13 cases studied. In situ hybridization analysis demonstrated the presence of vitronectin mRNA in cells present in areas rich in infiltrating inflammatory cells. The adherent population of the rheumatoid arthritic synovial cells was isolated and found to synthesize and secrete vitronectin into the medium (seven of 10 isolates), as assessed by metabolic labelling and immunoprecipitation. Plasmin-generating activity was detected in the adherent synovial cells, and this activity was increased by antibodies to vitronectin. Our findings show, for the first time, that vitronectin can be endogenously produced in a pathophysiological system where it can inhibit the generation of plasmin.

Keywords

vitronectin; plasmin; fibrinolysis; arthritis

Published in

British journal of rheumatology
1998, volume: 37, number: 6, pages: 620-629
Publisher: OXFORD UNIV PRESS

SLU Authors

• Pejler, Gunnar

  • Department of Veterinary Medical Chemistry, Swedish University of Agricultural Sciences
    

Associated SLU-program

Future Animal Health and Welfare (until Jan 2017)

UKÄ Subject classification

Biochemistry
Molecular Biology

Publication identifier

• DOI: https://doi.org/10.1093/rheumatology/37.6.620

Permanent link to this page (URI)

https://res.slu.se/id/publ/66613