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Interleukin-33 promotes proliferation and inhibits apoptosis of fibroblast-like synoviocytes in rheumatoid arthritis


1, 2, 3, 4, 5, 6

 

  1. Department of Immunology, Liaoning Institute of Basic Medicine, Shenyang, China. sywusuqin@163.com
  2. Department of Immunology, Liaoning Institute of Basic Medicine, Shenyang, China.
  3. Department of Obstetrics, Shenyang No.5 People’s Hospital, Shenyang, China.
  4. Department of Immunology, Liaoning Institute of Basic Medicine, Shenyang, China.
  5. Department of Anatomy, Liaoning Institute of Basic Medicine, Shenyang, China.
  6. Department of Clinical Pharmacy, China Medical University, Shenyang, China.

CER13061
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PMID: 33124566 [PubMed]

Received: 31/12/2019
Accepted : 17/07/2020
In Press: 09/10/2020

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.

Rheumatology Article