Long noncoding RNA HOXA-AS2 mediates microRNA-106b-5p to repress sepsis-engendered acute kidney injury.

Abstract

HOXA cluster antisense RNA 2 (HOXA-AS2) is a long noncoding RNA associated with the development of numerous cancers. But, whether HOXA-AS2 exhibits a certain function in sepsis-engendered acute kidney injury (AKI) remains uninvestigated. We strived to unveil the role of HOXA-AS2 in sepsis-engendered AKI. The expression of HOXA-AS2 in sepsis patients, animal models and lipopolysaccharide (LPS)-impaired HK-2 cells was primarily assessed via a real-time quantitative polymerase chain reaction. The effects of HOXA-AS2 on cell survival of HK-2 cells under LPS irritation were evaluated after overexpression of HOXA-AS2. The correlation between HOXA-AS2 and microRNA (miR)-106b-5p was forecasted via bioinformatics software and verified by using a luciferase report system. Subsequently, the functions of miR-106b-5p in LPS-damaged HK-2 cells were reassessed. Western blot was used for the determination of Wnt/β-catenin and nuclear factor-κB (NF-κB) pathways. HOXA-AS2 expression was decreased in sepsis patients, animal operation group and LPS-irritated HK-2 cells. Overexpressed HOXA-AS2 mollified LPS-triggered impairment in HK-2 cells. In addition, a negative mediatory relation between HOXA-AS2 and miR-106b-5p was predicated. Synchronously, overexpressed miR-106b-5p counteracted the protection of HOXA-AS2 in LPS-damaged HK-2 cells. Ultimately, Wnt/β-catenin and NF-κB pathways were hindered by HOXA-AS2 via targeting miR-106b-5p. HOXA-AS2 exhibited protection in sepsis-engendered AKI via targeting miR-106b-5p and hindering the Wnt/β-catenin and NF-κB pathways.