RRC ID 81180
Author Hu SL, Thadevoos LA, Ho TL, Lin YY, Chen HT, Huang CC, Su CM, Tang CH.
Title FGF23 facilitates IL-1β synthesis in rheumatoid arthritis through activating PI3K, Akt, and NF-κB pathways.
Journal Environ Toxicol
Abstract Rheumatoid arthritis (RA) is a well-known autoimmune disorder related with joint pain, joint swelling, cartilage and bone degradation as well as deformity. Fibroblast growth factor 23 (FGF23) is an endocrine factor of the FGF family primarily produced by osteocytes and osteoblasts, involves an essential effect in pathogenesis of RA. IL-1β is a vital proinflammatory factor in the development of RA. However, the role of FGF23 on IL-1β synthesis in RA has not been fully explored. Our analysis of database revealed higher levels of FGF23 and IL-1β in RA samples compared with healthy controls. High-throughput screening demonstrated that IL-1β is a potential candidate factor after FGF23 treatment in RA synovial fibroblasts (RASFs). FGF23 concentration dependently promotes IL-1β synthesis in RASFs. FGF23 enhances IL-1β expression by activating the PI3K, Akt, and NF-κB pathways. Our findings support the notion that FGF23 is a promising target in the remedy of RA.
Volume 39(6)
Pages 3283-3291
Published 2024-6-1
DOI 10.1002/tox.24180
PMID 38380842
MeSH Arthritis, Rheumatoid* / metabolism Cells, Cultured Female Fibroblast Growth Factor-23* Fibroblast Growth Factors / metabolism Fibroblasts* / drug effects Fibroblasts* / metabolism Humans Interleukin-1beta* / metabolism Male NF-kappa B / metabolism Phosphatidylinositol 3-Kinases / metabolism Proto-Oncogene Proteins c-akt / metabolism Signal Transduction* / drug effects Synovial Membrane / drug effects Synovial Membrane / metabolism
Resource
Human and Animal Cells MH7A(RCB1512)