Long non-coding RNA PVT1 regulates LPS-induced acute kidney injury in an model of HK-2 cells by modulating the miR-27a-3p/OXSR1 axis.

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.