Circ_0040994 depletion alleviates lipopolysaccharide‐induced HK2 cell injury through miR‐17‐5p/TRPM7 axis

Abstract

AbstractBackgroundSepsis is a fatal systemic inflammatory disease that causes septic acute kidney injury (AKI). In this work, we explored the roles of circ_0040994 in lipopolysaccharide (LPS)‐induced human kidney‐2 (HK2) cell injury.MethodsCirc_0040994, miR‐17‐5p and transient receptor potential melastatin 7 (TRPM7) expression were detected by qRT‐PCR. Cell functions were examined by MTT assay, flow cytometry assay, western blot, ELISA assay, and oxidative stress assay. The molecular association was detected by dual‐luciferase reporter assay.ResultsCirc_0040994 was upregulated in the serum of septic AKI patients in comparison with the serum of healthy controls. Silencing circ_0040994 enhanced cell viability but inhibited cell apoptosis, cell inflammation and oxidative stress in LPS‐triggered HK2 cells. Circ_0040994 acted as a miR‐17‐5p sponge to regulate the level of TRPM7. Moreover, miR‐17‐5p could alleviate LPS‐induced HK2 cell injury by suppressing TRPM7.ConclusionCirc_0040994 downregulation alleviated LPS‐induced HK2 cell injury through the miR‐17‐5p/TRPM7 axis.