CircTRHDE knockdown protects WI-38 cells against LPS-induced inflammatory injury

Abstract

Background

Circular RNAs (circRNAs) have been reported to be involved in the progression of infantile pneumonia. Here, we investigated the function of circTRHDE in lipopolysaccharide (LPS)-induced cell inflammatory injury to evaluate its role in infantile pneumonia progression.

Methods

The circTRHDE, microRNA (miR)-381-3p and TNF-receptor associated factor 3 (TRAF3) expression were detected by quantitative real-time PCR. LPS-induced WI-38 cells were used to construct an inflammatory injury model. Cell viability, inflammation and apoptosis were measured by cell counting kit assay, ELISA assay and flow cytometry. Caspase3 activity, MDA level and SOD activity were analysed to assess cell apoptosis and oxidative stress. Protein levels were determined using western blot analysis. The interaction between miR-381-3p and circTRHDE or TRAF3 was confirmed by dual-luciferase activity assay and RNA pull-down assay.

Results

CircTRHDE had increased expression in infantile pneumonia patients and LPS-induced WI-38 cells. LPS treatment inhibited WI-38 cell viability while promoting inflammation, apoptosis and oxidative stress. However, knockdown of circTRHDE remitted LPS-triggered WI-38 cell injury. CircTRHDE could sponge miR-381-3p to positively regulate TRAF3 expression. MiR-381-3p suppressed LPS-induced WI-38 cell inflammatory injury, and this effect was revoked by TRAF3 overexpression. Also, LPS-induced WI-38 cell inflammatory injury restrained by circTRHDE knockdown also were reversed by miR-318-3p inhibitor or TRAF3 overexpression.

Conclusion

Our findings demonstrated that circTRHDE might be a target for infantile pneumonia treatment, which relieved LPS-induced cell inflammatory injury by the regulation of the miR-318-3p/TRAF3 axis.

Keywords:

• Infantile pneumonia
• circTRHDE
• miR-381-3p
• TRAF3

Disclosure statement

The authors declare that they have no conflicts of interest.

Author contributions

All authors contributed to the study conception and design. Clinical data collection, genetic counselling and follow-up were performed by YZ and XC. Array data analyses was performed by JL and XS. The first draft of the manuscript was written by LS, and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.