Linc-KIAA1737-2 promoted LPS-induced HK-2 cell apoptosis by regulating miR-27a-3p/TLR4/NF-κB axis

Inflammation and renal cell apoptosis participate in sepsis-induced acute kidney injury. Previous research found the upregulation of long non-coding RNA Linc-KIAA1737-2 in hypoxia- or inflammation-challenged human proximal tubular epithelial cells, but its role in sepsis-induced acute kidney injury is underexplored. In this research, we found that Linc-KIAA1737-2 could be upregulated in HK-2 human proximal tubular epithelial cells by LPS treatment, and knock-down of this lncRNA significantly attenuated LPS-induced apoptosis in HK-2 cells, while its overexpression showed opposite effect. MiR-27a-3p was confirmed to interact with Linc-KIAA1737-2 in HK-2 cells by RNA pull-down and dual-luciferase assay. MiR-27a-3p mimic transfection significantly attenuated LPS-induced HK-2 cell apoptosis by downregulating the protein levels of TLR4 and NF-kappa B, which was overturned by overexpression of Linc-KIAA1737-2. Our results suggested that Linc-KIAA1737-2 could promote LPS-induced apoptosis in HK-2 cells, and presumably sepsis-induced acute kidney injury, by regulating the miR-27a-3p/TLR4/NF-kappa B axis.

Automated summary

In this study, upregulation of Linc-KIAA1737-2 was found to promote LPS-induced apoptosis in HK-2 cells, while transfection with miR-27a-3p mimic could attenuate LPS-induced cell apoptosis. These findings suggest a potential role for Linc-KIAA1737-2 in sepsis-induced acute kidney injury through the regulation of the miR-27a-3p/TLR4/NF-kappa B axis.