LncRNA cardiac autophagy inhibitory factor is downregulated in rheumatoid arthritis and suppresses the apoptosis of fibroblast-like synoviocytes by promoting the maturation of miRNA-20a

Abstract

Objectives: In this study, we aimed to investigate the effects of LncRNA cardiac autophagy inhibitory factor (CAIF) and miR-20a on the apoptosis of synovial cells in rheumatoid arthritis (RA) and the regulatory mechanism.

Patients and methods: Between May 2018 and March 2020, a total of 62 RA patients (24 males, 38 females; mean age: 55.2±4.9 years; range, 42 to 68 years) and 62 controls (24 males, 38 females; mean age: 55.3±4.8 years; range, 41 to 68 years) were included in this study. Plasma samples were collected from all participants. The expression levels of CAIF, mature miR-20a, and miR-20a precursor in these plasma samples were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Correlations were analyzed using linear regression analysis. Overexpression of CAIF was achieved in human fibroblast-like synoviocytes (HFLSs) and the expression levels of mature miR-20a and miR-20a precursor were determined using RT-qPCR. Cell apoptosis was analyzed by cell apoptosis assay.

Results: The CAIF was downregulated in RA and positively correlated with the expression of mature miR-20a. In HFLSs, LPS treatment resulted in downregulation of both CAIF and miR-20a in a dose-dependent manner. In HFLSs, overexpression of CAIF did not affect the expression of miR-20a precursor, but upregulated the expression of mature miR-20a. Cell apoptosis analysis showed that overexpression of CAIF and miR-20a inhibited the apoptosis of HFLSs induced by LPS. The combination of overexpression of CAIF and miR-20a showed a stronger effect.

Conclusion: The CAIF may suppress the apoptosis of HFLSs in RA by promoting the maturation of miR-20a.

Citation: Xu D, Lin L, Chen Z. LncRNA cardiac autophagy inhibitory factor is downregulated in rheumatoid arthritis and suppresses the apoptosis of fibroblast-like synoviocytes by promoting the maturation of miRNA-20a. Arch Rheumatol 2022;37(3):383-392.

The study protocol was approved by the Ethics Committee of the second affiliated hospital of Fujian Medical University (Date: 2018, no: LCS18057). The study was conducted in accordance with the principles of the Declaration of Helsinki.

A written informed consent was obtained from each participant.

Data Sharing Statement:
The data that support the findings of this study are available from the corresponding author upon reasonable request.

Study concepts, study design, literature research, experimental studies, manuscript preparation and editing: D.X.; Literature research, experiments work and manuscript writing: L.L., Z.C.

The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.

This work was funded by the General project of Natural Science Foundation of Fujian Province (Grant No. 2021J01248) and the Nursery Fund of the Second Affiliated Hospital of Fujian Medical University.