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

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.