LncRNA H19 activates cell pyroptosis via the miR-22-3p/NLRP3 axis in pneumonia.

ABSTRACT

OBJECTIVE: Pneumonia is an infectious pulmonary disease with a high morbidity and mortality. It has been reported that multiple long noncoding RNAs (LncRNAs) are involved in the progression of pneumonia, such as LncRNA SNHG16. However, the role and underlying mechanism of LncRNA H19 in the pyroptosis of pneumonia has not been elucidated. The purpose of this research was to explore the mechanism by which LncRNA H19 regulates LPS-induced pneumonia in WI-38 cells. METHODS: An LPS induced pneumonia model in WI-38 cells was established. Total RNA extracted from WI-38 cells was analyzed using RT-qPCR, and the total proteins isolated from the WI-38 cells were analyzed using Western blotting. MTT assays, TUNEL staining, bioinformatics, and luciferase reporter assays were subsequently conducted. RESULTS: In the LPS induced pneumonia model, LncRNA H19 silences inhibited LPS-induced WL-38 cell pyroptosis, and LncRNA H19 overexpression promotes LPS-induced WL-38 cell pyroptosis. Also, LncRNA H19 acts as a sponge of miR-22-3p, which targets NLRP3, and NLRP3 attenuates the effect of LncRNA H19 silencing on LPS-induced WL-38 cell pyroptosis. CONCLUSION: Our data demonstrated the roles and potential mechanisms of LncRNA H19 in the regulation of pneumonia cell pyroptosis, indicating that LncRNA H19 is an efficient predictive and curative target for pneumonia.