https://orcid.org/0000-0003-4388-7468
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Abstract
Objective
To explore the effect of CD5-like molecule (CD5L) on rheumatoid arthritis (RA) fibroblast-like synoviocytes (RA-FLS) and the relative molecular mechanism of CD5L in it.
Methods
Recombinant protein CD5L was used to stimulate the cultured RA-FLS cells. The inflammation-related cytokines were determined by real time-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). The signal molecules and apoptosis-related molecules were detected by western blot assay (WB), and cell counting kit-8 (CCK-8) was used to detect the proliferation.
Results
CD5L can increase the production of IL-6, IL-8, and TNF-α and this effect can be inhibited by signal pathway inhibitor. At the same time, CD5L activated ERK1/2 MAPK signal, inhibitor treatment can weaken the intensity of phosphorylation. In addition, CD5L can enhance the proliferation ability of RA-FLS.
Conclusion
CD5L induces the production of inflammatory cytokines in RA-FLS through the ERK1/2 MAPK pathway and increases cell survival.
Acknowledgements
We thank the Clinical Laboratory of the Department of Medical Laboratory and the Medical Experimental Center of the First Affiliated Hospital of Chongqing Medical University for their equipment and technical support.
Data availability
The datasets used and/or analysed during the current study available from the corresponding author on reasonable request.
Disclosure statement
The authors declare no conflict of interest.
Author contribution
Huiqing Yang carried out the major experiments and wrote the main manuscript text. Yan Luo provided technical and academic guidance. Xiaofei Lai modified the manuscript and provided financial support. All authors reviewed the manuscript.