Long non‑coding RNA PVT1 regulates LPS‑induced acute kidney injury in an in vitro model of HK‑2 cells by modulating the miR‑27a‑3p/OXSR1 axis
- Qian Yang
- Qi Sun
- Ping Jin
Affiliations: Department of Critical Care Medicine, Jingzhou Central Hospital, The Second Clinical Medical College, Yangtze University, Jingzhou, Hubei 434000, P.R. China
- Published online on: July 1, 2022 https://doi.org/10.3892/etm.2022.11490
Copyright: © Yang
et al. This is an open access article distributed under the
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Sepsis is a severe inflammatory disease caused by infection that can lead to multiple organ failure. Acute kidney injury (AKI) is considered to be a major cause of septic mortality in infected organs. Previous studies have revealed that non‑coding RNAs are involved in AKI, but the underlying mechanisms are mostly unknown. The present study aimed to explore the role of long non‑coding RNA plasmacytoma variant translocation gene 1 (lncRNA PVT1) in lipopolysaccharide (LPS)‑induced acute kidney injury and the underlying mechanism. In the present study, reverse transcription‑quantitative PCR analysis indicated that, in HK‑2 cells treated with LPS, the mRNA expression levels of lncRNA PVT1 and oxidative stress responsive kinase 1 (OXSR1) were upregulated, and the expression of microRNA (miR)‑27a‑3p was downregulated. Furthermore, LPS treatment could promote the secretion of tumor necrosis factor (TNF)‑α and interleukin (IL)‑6, inhibit cell proliferation and induce apoptosis, which was rescued by PVT1 knockdown. Dual‑luciferase reporter assay, RIP assay and pull‑down assay results demonstrated that miR‑27a‑3p may be a target miR of PVT1, and that OXSR1 is the target gene of miR‑27a‑3p. Moreover, it was found that miR‑27a‑3p overexpression decreased the secretion of TNF‑α and IL‑6, promoted cell proliferation and inhibited apoptosis in LPS‑treated HK‑2 cells, which could be reversed by OXSR1 overexpression. Therefore, the present results indicated that lncRNA PVT1 regulated inflammatory cytokine secretion, cell proliferation and apoptosis by targeting miR‑27a‑3p, and modulating OXSR1 expression in LPS‑induced HK‑2 cells.