miR‑122‑5p downregulation attenuates lipopolysaccharide‑induced acute lung injury by targeting IL1RN
- Jie Li
- Xiaoxia Zeng
- Weiqing Wang
Affiliations: Department of Pulmonary Disease, Hubei Hospital of Traditional Chinese Medicine, Wuhan, Hubei 430000, P.R. China, Department of Emergency, Hubei Hospital of Traditional Chinese Medicine, Wuhan, Hubei 430000, P.R. China
- Published online on: September 8, 2021 https://doi.org/10.3892/etm.2021.10713
Copyright: © Li
et al. This is an open access article distributed under the
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MicroRNAs (miRs) and inflammatory cytokines can induce acute lung injury (ALI), which can develop into acute respiratory distress syndrome in severe cases. Previous research has revealed that miR‑122‑5p participates in the development of ALI, and that its expression is positively associated with ALI. However, the mechanism by which miR‑122‑5p contributes to ALI remains to be determined. In the current study, TargetScan and dual luciferase reporter gene assays were used to confirm that IL‑1 receptor antagonist (IL1RN) was a target of miR‑122‑5p. Subsequently, by referring to previous literature, a lipopolysaccharide (LPS)‑induced ALI cell model was established. A549 cells were transfected with mimic control or miR‑122‑5p mimics for 24 h, and 10 µg LPS was used to treat the transfected cells for 12 h. The results revealed that miR‑122‑5p mimics decreased cell viability and promoted apoptosis. Lactate dehydrogenase (LDH) release assays indicated that miR‑122‑5p mimics increased LDH release. ELISA demonstrated that miR‑122‑5p mimics promoted TNF‑α, IL‑1β and IL‑6 expression levels. A549 cells were transfected with inhibitor control, miR‑122‑5p inhibitor, miR‑122‑5p inhibitor + control‑small interfering (si)RNA or miR‑122‑5p inhibitor + IL1RN‑siRNA for 24 h, after which the cells were treated with 10 µg LPS for 12 h. The results revealed that the effects of the miR‑122‑5p inhibitor were the opposite of those of the miR‑122‑5p mimic. All the effects of miR‑122‑5p inhibitor on LPS‑treated A549 cells were significantly reversed by IL1RN‑siRNA. Overall, the results highlighted miR‑122‑5p as a potential novel target for the treatment of ALI.