Inhibition of microRNA-155 alleviates lipopolysaccharide-induced kidney injury in mice

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Accumulated evidences suggest that microRNAs (miRNAs) are related with inflammation-associated diseases. The aim of this study is to investigate whether miR-155 is involved in lipopolysaccharide (LPS)-induced kidney injury, and to explore the underlying mechanisms. Mice were intraperitoneally injected with LPS to construct endotoxemia mice model, and miR-155 inhibitor was injected via tail vein to suppress the expression of miR-155 in kidney. The results indicated that the expression of miR-155 was markedly increased in renal tissues of LPS-treated mice. And miR-155 inhibitor protected mice from LPS-induced kidney injury associated with the lower levels of TNF-α and IL-6 in renal tissues. Furthermore, inhibition of miR-155 increased the expression of suppressor of cytokine signaling 1 (SOCS1), a target gene of miR-155 and a negative regulator of Janus activated kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway. Consistently, inhibition of miR-155 suppressed the expression of JAK2, STAT3 and phosphorylated STAT3 (p-STAT3). All these results indicated that inhibition of miR-155 protects mice from LPS-induced kidney injury possibly through regulating SOCS1-JAK2/STAT signaling pathway, which suggested that miR-155 might be an important and potential target in developing therapy for preventing sepsis-associated kidney injury.