Concise reports
Rheumatoid synovial endothelial cells secrete decreased levels of
tissue inhibitor of MMP (TIMP1)
Sutton Arthritis Research Laboratory, Department of
Rheumatology, Royal North Shore Hospital, St Leonards NSW, Australia
Correspondence to: Dr C Jackson, Sutton Arthritis Research Laboratory, Department of Rheumatology, University of Sydney at Royal North Shore Hospital, St Leonards NSW, 2065, Australia.
Accepted for publication 23
January 1998
OBJECTIVES
Angiogenesis (the formation of
new blood vessels) is a major component of the inflammatory pannus in
rheumatoid arthritis (RA). Matrix metalloproteinase (MMP) secretion by
microvascular endothelial cells is an essential step in angiogenesis.
The secretion of MMP1, MMP2, MMP9, and TIMP1 by human microvascular
endothelial cells derived from RA synovium (RASE) to normal synovium
(NSE) and neonatal foreskin (FSE) was compared.
METHODSConfluent monolayers of endothelial
cells in basal medium were pre-incubated for 24 hours in the presence
or absence of phorbol myristate acetate (PMA, 100 ng/ml). MMP1 activity
was measured using a spectrophotometric assay and western blotting.
MMP2 and MMP9 were measured using zymography. TIMP1 was measured by
enzyme linked immunosorbent assay and western blotting.
RESULTSThere was little difference between
the amounts of MMP2 secreted by any of the cell lines. In response to
PMA both synovial cell types showed a significantly higher MMP1 and
MMP9 activity compared with FSE, although there was no difference
between RASE and NSE. Tumour necrosis factor 
had minimal effect on
MMP activity. There was a striking decrease in the amount of TIMP1
secreted by RASE compared with normal synovium.
CONCLUSIONSAs overall MMP activity is a balance
between the amount of MMP and TIMP1 present, the low levels of TIMP1
produced by RASE would shift the balance in favour of increased MMP
activity by these cells. This is likely to contribute to the angiogenic
potential of RASE.
© 1998 by Annals of the Rheumatic Diseases
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