CXCL7 enhances RANKL-induced osteoclastogenesis via the activation of ERK/NFATc1 signaling pathway in inflammatory arthritis
Authors' conclusion
CXCL7 contributes to the bone erosion in RA by enhancing RANKL-induced osteoclastogenesis via the activation of ERK/NFATc1 signaling pathways.
Study context
- Population
- Rheumatoid arthritis (RA) patients and healthy controls; mice with collagen-induced arthritis (CIA)
- Comparison
- ACPA+ RA vs ACPA− RA vs healthy controls (plasma CXCL7); Cxcl7 neutralizing antibody in CIA mice
Methodological detailsEnzyme-linked immunosorbent assay (ELISA), tartrate-resistant acid phosphates (TRAP) staining and F-actin ring immunofluorescence, Western blotting, CIA mouse model with Cxcl7 neutralizing antibodies, histopathology and micro-computed tomography (micro-CT)
- ELISA
- TRAP staining and F-actin ring immunofluorescence
- Western blotting
- CIA mouse model with Cxcl7 neutralizing antibodies
- Histopathology and micro-CT
Main finding
As reported in the abstract
- Plasma CXCL7 significantly higher in ACPA+ RA vs ACPA− RA and healthy controls
- CXCL7 level positively correlated with disease activity and bone erosion in RA
- CXCL7 promoted RANKL-induced osteoclastogenesis in CD14+ monocytes from RA patients
- Cxcl7 significantly enhanced RANKL-induced ERK1/2 phosphorylation and NFATc1 expression
- Cxcl7 neutralizing antibody alleviated arthritis severity in CIA, reducing inflammation, osteoclast numbers and bone destruction
Original publication
CXCL7 enhances RANKL-induced osteoclastogenesis via the activation of ERK/NFATc1 signaling pathway in inflammatory arthritis. Arthritis Res Ther. Published 15 February 2025. doi:10.
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