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Background: Rheumatoid arthritis (RA) is a common immune -mediated chronic inflammatory disease that can cause joint damage and deformity
.
Current treatments include antirheumatic drugs aimed at suppressing systemic immunity
Common immune -mediated chronic inflammatory diseases that can cause joint damage and deformity of immunity .
Methods: Immunohistochemistry and qRT-PCR were used to analyze the synovial tissue of RA patients and mice with antigen-induced arthritis (AIA)
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Pdgfrα-CreER and Gdf5-Cr mice were targeted, hybridized with fluorescent reporters for cell tracking, and Yap-flox mice were subjected to conditional Yap ablation
RESULTS: Yap, its binding partner Snail and downstream target connective tissue growth factor were up-regulated in proliferative human RA and mouse AIA synovium, and Yap was detected in SF but not in macrophages
.
Lineage tracing revealed that Pdgfrα-expressing SFs expanded polyclonally during AIA, with expansion of Gdf5-lineage SF subsets primarily from the embryonic interarticular region
Conclusions: Our findings do not reveal the IL-6-YAP-Snail signaling axis of pathogenic SF in osteoarthritis
Our discovery and revelation of the IL-6-YAP-Snail signaling axis of pathogenic SF in osteoarthritis
Original source: Symons RA, Colella F, Collins FL, et al.
Targeting the IL-6-Yap-Snail signalling axis in synovial fibroblasts ameliorates inflammatory arthritis.
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