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) |