LINC00261 relieves the progression of sepsis-induced acute kidney injury by inhibiting NF-κB activation through targeting the miR-654-5p/SOCS3 axis.

Sepsis is a life-threatening disease, which can cause the dysfunction of multiple organs, including kidney. Recently, a number of studies found that the long non-coding RNA (lncRNA) is closely associated with the development and progression of sepsis; however, the role of long intergenic non-protein coding RNA 261 (LINC00261) in sepsis-induced acute kidney injury is poorly understood. In this study, we found the expression of LINC00261 was significantly decreased in the serum of patients with sepsis than healthy controls. A similar result was also observed in the mouse model of sepsis induced by lipopolysaccharide (LPS). Further investigations revealed that overexpression of LINC00261 improved the viability, suppressed the apoptosis and reduced the generation of inflammatory cytokines in LPS-treated HK-2 cells. Mechanistically, we confirmed that LINC00261 could function as a sponge to combine with microRNA-654-5p (miR-654-5p) which inhibits nuclear factor-κB (NF-κB) activity by targeting suppressor of cytokine signaling 3 (SOCS3). In conclusion, our results demonstrate that LINC00261 may regulate the progression of sepsis-induced acute kidney injury via the miR-654-5p/SOCS3/NF-κB pathway and therefore provides a new insight into the treatment of this disease.