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Volume 272, Number 50, Issue of December 12, 1997
pp. 31504-31509
(Received for publication, April 18, 1997, and in revised form, August 28, 1997)
From the Neutrophil collagenase (matrix
metalloproteinase-8 or MMP-8) is regarded as being synthesized
exclusively by polymorphonuclear neutrophils (PMN). However, in
vivo MMP-8 expression was observed in mononuclear fibroblast-like
cells in the rheumatoid synovial membrane. In addition, we detected
MMP-8 mRNA expression in cultured rheumatoid synovial fibroblasts
and human endothelial cells. Up-regulation of MMP-8 was observed after
treatment of the cells with either tumor necrosis factor-
Matrix Metalloproteinase-8 Is Expressed in Rheumatoid Synovial
Fibroblasts and Endothelial Cells
REGULATION BY TUMOR NECROSIS FACTOR-
AND DOXYCYCLINE
,
,
,
,
,
,
Gaubius Laboratory TNO-PG, 2301 CE Leiden,
The Netherlands, the Departments of § Periodontology and
Medical Chemistry, and ¶ Anatomy, University of Helsinki,
FIN-00014, Helsinki, Finland, 
Oulu University Hospital, Medix Biochemica Oy Ab, Kauniainen,
Finland, and the §§ Department of Biochemistry,
Faculty of Chemistry, University of Bielefeld,
33 501 Bielefeld, Germany
(10 ng/ml)
or phorbol 12-myristate 13-acetate (10 nM). Western
analysis showed a similar regulation at the protein level. The size of
secreted MMP-8 was 50 kDa, which is about 30 kDa smaller than MMP-8
from PMN. Conditioned media from rheumatoid synovial fibroblasts
contained both type I and II collagen degrading activity. However,
degradation of type II collagen, but not that of type I collagen, was
completely inhibited by 50 µM doxycycline, suggesting
specific MMP-8 activity. In addition, doxycycline down-regulated MMP-8
induction, at both the mRNA and protein levels. Thus MMP-8 exerts
markedly wider expression in human cells than had been thought
previously, implying that PMN are not the only source of cartilage
degrading activity at arthritic sites. The inhibition of both MMP-8
activity and synthesis by doxycycline provides an incentive for further
studies on the clinical effects of doxycycline in the treatment of
rheumatoid arthritis.
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