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Expression of TREM-2 and its inhibitory effects on TNF-α induced inflammation in fibroblast-like synoviocytes via inhibiting p38 pathway activation
S.H. Huang1, G.W. Liu2, J.H. Li3, J.H. Xu4, D.W. Xu5, W.Q. Zhang6, J.R. Huang7
- Department of Orthopaedics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou; Department of Orthopaedics, the Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China.
- Department of Orthopaedics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou; Department of Orthopaedics and Traumatology, Qingyuan People’s Hospital, The Sixth Affiliated Hospital of Guangzhou Medical University, Guangdong, China.
- Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou Medical University, Guangdong, China.
- Department of Orthopaedics, Zengcheng District People’s Hospital, Guangzhou, China.
- Department of Orthopaedics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
- Department of Orthopaedics, Zengcheng District People’s Hospital, Guangzhou, China.
- Department of Orthopaedics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou; Department of Orthopaedics, Zengcheng District People’s Hospital, Guangzhou, China. guke16@163.com
CER10356
2018 Vol.36, N°2
PI 0185, PF 0194
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PMID: 28869414 [PubMed]
Received: 22/02/2017
Accepted : 29/05/2017
In Press: 31/08/2017
Published: 05/02/2018
Abstract
OBJECTIVES:
It is not clear whether TREM-2 (the “triggering receptor expressed on myeloid cells 2”) is expressed in fibroblast-like synovial cells (FLSs). In this study, we aimed to determine the expression of TREM-2 in rheumatoid arthritis (RA)-FLSs and explore whether and how TREM-2 modulates the function of RA-FLSs.
METHODS:
Western blot and RT-PCR were used to detect the expression of TREM-2 in RA-FLSs, siRNA and lentivirus were used to down-regulate and up-regulate the expression of TREM-2 in RA-FLSs. Then mRNA expression of IL-1β, IL-6, and MMP-13 was determined by RT-qPCR. Protein secretion of IL-1β, IL-6, and MMP-13 in the supernatant was determined by ELISA assay; expression of cell signal transduction molecules was determined by western blot.
RESULTS:
A: Relative to OA-FLSs, mRNA and protein expression levels of TREM-2 in RA-FLSs are significantly elevated. TREM-2 protein is mainly expressed in the cytoplasm of RA-FLSs; B: In RA, the expression of TREM-2 was reduced at first and then up-regulated after stimulation by TNF-α. TREM-2 also inhibited the activation of TNF-α induced of inflammation in RA-FLSs by the p38 pathway, which regulates the production of cytokines and matrix metalloproteinases.
CONCLUSIONS:
TREM-2 expressed in RA-FLSs and TNF-α mediated reduction of inflammatory reactions. These phenomena indicated that TREM-2 may be a potential target in the treatment of RA.
