Interleukin-22 promotes proliferation of fibroblast-like synoviocytes from patients with rheumatoid arthritis by inducing STAT3 phosphorylation
ZHU Junqing
WANG Ran
CHEN Shixian
ZHAO Di
LI Juan
Abstract：Objective To clarify the mechanism by which interleukin-22 (IL-22) promotes the proliferation of fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthritis (RA). Methods FLS were isolated from the synovial tissues of patients with RA and identified by immunohistochemistry for vimentin/CD68.The cells were subcultured and incubated with different concentrations of IL-22 for 24,48,or 72 h,and their proliferation was examined using MTT assay.After treatment of the cells with IL-22 and AG490,alone or in combination,the expressions of the total and phosphorylated proteins of STAT3, ERK1/2 and P38 were detected with Western blotting. Results IL-22 significantly increased the proliferation of FLS in a dose-dependent manner(P<0.05).The total protein of STAT3 in the cells showed no significant changes with extended time of IL-22 treatment(P=0.68),but the expression of phosphorylated STAT3 protein increased significantly(P<0.001).The total and phosphorylated proteins of ERK1/2 and P38 underwent no significant changes after IL-22 treatment (P>0.05). A combined treatment with 50 ng/mL IL-22 and 100 μmol/L AG490 resulted in a significant decrease in the proliferation of FLS as compared with IL-22 treatment alone(P<0.01).Conclusion IL-22 can dose-dependently promote the proliferation of FLS from patients with RA by inducing phosphorylation of STAT3 protein but not through ERK1/2 or P38 signal pathway.
Keywords：rheumatoid arthritisfibroblast-like synoviocytesinterleukin-22signaling pathway
Publication Date：2017-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：7( 1570-1576 )