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

BackgroundSepsis 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.

Automated summary

In this study, the role of circ_0040994 in lipopolysaccharide-induced acute kidney injury was investigated. The results showed that circ_0040994 was upregulated in the serum of septic AKI patients. Silencing circ_0040994 could enhance cell viability and inhibit cell apoptosis, inflammation, and oxidative stress. Furthermore, circ_0040994 acted as a sponge for miR-17-5p to regulate the levels of TRPM7, and miR-17-5p could alleviate LPS-induced cell injury by suppressing TRPM7.