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Arthritis Biology, Department of Arthritis and Bone Metabolism, Novartis Pharma AG, Basle, Switzerland;
Arcus Sportklinik, Pforzheim, Germany; and
Novartis Institute for Biomedical Research, Functional Genomics, Novartis Pharmaceuticals Corporation, Summit, NJ 07901
The acute-phase reactant rabbit serum amyloid A 3
(SAA3) was identified as the major difference product in
Ag-induced arthritis in the rabbit, a model resembling in many aspects
the clinical characteristics of rheumatoid arthritis (RA) in humans. In
Ag-induced arthritis, up-regulated SAA3 transcription in
vivo was detected in cells infiltrating into the inflamed joint, in the
area where pannus formation starts and, most notably, also in
chondrocytes. The proinflammatory cytokine IL-1
induced
SAA3 transcription in primary rabbit chondrocytes in
vitro. Furthermore, rSAA3 protein induced transcription of matrix
metalloproteinases in rabbit chondrocytes in vitro. In the human
experimental system, IL-1 induced transcription of acute-phase SAA
(A-SSA; encoded by SAA1/SAA2) in primary chondrocytes.
Similar to the rabbit system, recombinant human A-SAA protein was able
to induce matrix metalloproteinases’ transcription in chondrocytes.
Further, immunohistochemistry demonstrated that A-SAA was highly
expressed in human RA synovium. A new finding of our study is that
A-SSA expression was also detected in cartilage in osteoarthritis. Our
data, together with previous findings of SAA expression in RA synovium,
suggest that A-SAA may play a role in cartilage destruction in
arthritis.
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