Full Papers
Interleukin-33 promotes proliferation and inhibits apoptosis of fibroblast-like synoviocytes in rheumatoid arthritis
S. Wu1, Y. Jiang2, Y. Teng3, X. Liu4, L. Zhou5, W. Li6
- Department of Immunology, Liaoning Institute of Basic Medicine, Shenyang, China. sywusuqin@163.com
- Department of Immunology, Liaoning Institute of Basic Medicine, Shenyang, China.
- Department of Obstetrics, Shenyang No.5 People’s Hospital, Shenyang, China.
- Department of Immunology, Liaoning Institute of Basic Medicine, Shenyang, China.
- Department of Anatomy, Liaoning Institute of Basic Medicine, Shenyang, China.
- Department of Clinical Pharmacy, China Medical University, Shenyang, China.
CER13061
2021 Vol.39, N°4
PI 0844, PF 0851
Full Papers
PMID: 33124566 [PubMed]
Received: 31/12/2019
Accepted : 17/07/2020
In Press: 09/10/2020
Published: 08/07/2021
Abstract
OBJECTIVES:
The aim of our study was to determine the effect of interleukin (IL)-33 on the proliferation, apoptosis, and secretion of inflammatory cytokines by fibroblast-like synoviocytes (FLSs) in rheumatoid arthritis (RA) and to investigate the underlying mechanisms.
METHODS:
Cultured RA FLSs and osteoarthritis (OA) FLSs were cocultured with different concentrations of IL-33. TUNEL assay and flow cytometry were used to detect apoptosis. Western blotting and Real-time (RT)-PCR were used to detect the expression levels of B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax), while the Cell Counting Kit-8 was used to determine cell proliferation in each cocultured group. Enzyme-linked immunosorbent assay was used to detect the expression levels of tumour necrosis factor (TNF)-α and IL-6 in the supernatant from each cell culture. Western blot analysis was used to determine the phosphorylated expression levels of the nuclear factor-kappa light chain enhancer of the activated B cells (NF-κB) pathway in each group.
RESULTS:
IL-33 inhibited RA FLS apoptosis, promoted FLS proliferation, increased Bcl-2 protein expression levels, and decreased Bax protein expression levels. It also increased the expression levels of inflammatory cytokines TNF-α and IL-6 and increased the expression levels of P-NF-κ B in FLSs.
CONCLUSIONS:
IL-33 inhibited apoptosis and promoted proliferation of FLSs; in addition, IL-33 increased the serum levels of inflammatory cytokines. The effect of IL-33 on RA FLSs was likely mediated via the NF-κB pathway.
