Intra-articular overexpression of oncostatin M (OSM) with either IL-1 or tumour necrosis factor alpha (TNF-α) increases RANK/RANKL expression in murine joints
Taken from "A model of inflammatory arthritis highlights a role for oncostatin M in pro-inflammatory cytokine-induced bone destruction via RANK/RANKL"
Arthritis Research & Therapy 2004;7(1):R57-R64.
Published online 10 Nov 2004
Copyright © 2004 Hui et al., licensee BioMed Central Ltd.Mice were injected intra-articularly with adenoviral vectors as described in Fig. 1, and the animals were sacrificed at day 7 following administration. Sections (= 4 per treatment group) were immunolocalized with antibodies specific for –RANK or –RANKL with haematoxylin counterstaining. No positive staining (brown) was observed in the controls (a and g), while similar patterns of RANK and RANKL staining were observed in the synovium and inflammatory cells in joints treated with a single cytokine (representative data are shown: (b) TNF-α, (h) IL-1). This expression was further enhanced by the combinations of OSM + IL-1 (c, e, i, k) or OSM + TNF-α (d, f, j, l), especially at sites of bone erosion (arrows). A marked increase in RANK and RANKL expression was also seen in the articular chondrocytes for both cytokine combinations (e, f, k, l). b, bone; bm, bone marrow; c, cartilage; i, inflammatory cells; s, synovial cells. Bar = 50 μm.