gms | German Medical Science

67. Jahrestagung der Deutschen Gesellschaft für Unfallchirurgie
89. Tagung der Deutschen Gesellschaft für Orthopädie und Orthopädische Chirurgie
44. Tagung des Berufsverbandes der Fachärzte für Orthopädie

11. bis 16.11.2003, Messe/ICC Berlin

The role of VEGF (Vascular Endothelial Growth Factor) in Osteoarthritis

Meeting Abstract (DGOOC 2003)

  • corresponding author Thomas Pufe - Department of Anatomy, Olshausenstrasse 40, 24098, Kiel, Phone: 0431 880 3087, Fax: 0431 880 1557
  • W. Petersen - Orthopaedic Surgery; Christian-Albrechts-University Kiel; Germany;
  • R. Mentlein - Department of Anatomy and
  • B. Kurz - Department of Anatomy and
  • M.B. Goldring - New England Baptist Bone & Joint Institute, Harvard Institue of Medicine, Boston MA
  • B. Tillmann - Department of Anatomy and

Deutsche Gesellschaft für Unfallchirurgie. Deutsche Gesellschaft für Orthopädie und orthopädische Chirurgie. Berufsverband der Fachärzte für Orthopädie. 67. Jahrestagung der Deutschen Gesellschaft für Unfallchirurgie, 89. Tagung der Deutschen Gesellschaft für Orthopädie und Orthopädische Chirurgie und 44. Tagung des Berufsverbandes der Fachärzte für Orthopädie. Berlin, 11.-16.11.2003. Düsseldorf, Köln: German Medical Science; 2003. Doc03dguO28-6

The electronic version of this article is the complete one and can be found online at:

Published: November 11, 2003

© 2003 Pufe et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.




In recent studies we have shown, that vascular endothelial growth factor (VEGF) is expressed in osteoarthritic but not in normal cartilage. Aim of this investigation was to analyse the function of VEGF in osteoarthritis (OA).

Methods & results

Immortalized human chondrocytes, which were a model, expressed VEGF and VEGFR-2. As evidenced by real time RT-PCR, VEGFR-2 expression was upregulated by VEGF itself. Stimulation of VEGFR-2 by the ligand resulted in autophosphorylation of the receptor, subsequent phosphorylation of the mitogen-activated protein kinases Erk ½ and finally the activation of the transcription factor AP-1 (activator protein-1) as shown by Western-Blot and electrophoretic mobility shift assay (EMSA). As consequence, VEGF raised the expression of active matrix metalloproteinase-1 (MMP-1) in culture supernatants. Also, chondrocyte proliferation was stimulated by VEGF.


The increased expression of the matrix metalloproteinases leads to a destruction of collagen and the successfully activated MAP-kinase pathway culminates in the expression of proinflammatory cytokines. The more intense proliferation comes along with a reduced coIlagen type II production. In conclusion, VEGF is participated in the osteoarthritic degradation of cartilage.