MiRNA-20a suppressed lipopolysaccharide‐induced HK‐2 cells injury via NFκB and ERK1/2 signaling by targeting CXCL12

Abstract

Acute kidney injury (AKI) has one of the highest mortalities in terms of inflammatory sepsis. MiR-20a is involved in a variety of inflammatory reactions, but its role in AKI remains unknown. The purpose of this study was to investigate specific in vitro function and mechanisms of miR‐20a in AKI. We used, lipopolysaccharide (LPS) against human proximal tubular epithelial (HK-2) cells to induce an in vitro model of AKI. Then, our data showed that miR-20a expression levels were down-regulated in LPS-treated HK-2 cells. Overexpression of miR-20a promoted cell viability, inhibited apoptosis rate and inhibited the expression of apoptotic factors and inflammatory cytokines in HK-2 cells after LPS stimulation. In addition, CXCL12 was identified as a direct target of miR-20a by luciferase reporter gene assay, and CXCL12 expression was negatively regulated by miR-20a. Moreover, CXCR4 attenuated the suppression of miR-20a on inflammation and apoptosis in LPS-stimulated HK-2 cells, and further data indicated that miR-20a deactivated CXCL12/CXCR-4, NFκB and ERK1/2 signaling by targeting CXCL12. Therefore, our data revealed that miR-20a may play an anti-inflammatory and antiapoptotic roles in LPS-induced HK-2 cells via deactivation of CXCL12/CXCR-4, NFκB and ERK1/2 signaling.