Investigation for the pathogenesis of secondary amyloidosis complicated with rheumatoid arthritis

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#1 Induction of COX-2 by β2-microglobulinβ2-microglobulin treatment increased the induction of COX-2 mRNA and COX-2 protein synthesis from human rheumatoid synovial cells in a dose-dependent manner. Dexamethasone suppressed the induction of COX-2 mRNA and protein in β2-microglobulin-stimulated synovial cells. These data indicated that COX-2 expression by β2-micoglobulin may be an important inflammatory process in hemodialysis associated osteoaithropathy.#2 Impaired degradation of serum amyloid A protein by cytokine-stimulated monocytes.CD14+ monocytes degraded SAA completely in vitro. When CD14* monocytes were pretreated with IL-1 β or IFN-γ, increasing amounts of SAA-related derivatives were detected in culture supernatants. This down-regulated proteolysis of SAA protein by cytokine stimulated monocytes may play a role in the mechanism of impaired SAA metabolism.