miR-27a suppresses TLR4-induced renal ischemia-reperfusion injury

Ischemia reperfusion injury (IRI) is one of the primary causes of acute renal injury and even acute renal failure. An increasing body of evidence has indicated that the aberrant expression of microRNAs (miRNA/miR) is closely associated with the progression of IRI. In the process of renal IRI, inflammatory reactions, cell adhesion and the death of renal tubular epithelial cells serve important roles. The present study investigated the expression of renal miRNAs following renal IRI in an attempt to identify the miRNAs that exert pivotal functions in renal IRI. The present study revealed that miR-27a, which was downregulated in IRI, and the 3′-untranslated region (UTR) of Toll-like receptor 4 (TLR4) have associated binding sites. The levels of TLR4, miR-27a and specific associated proteins in the renal tissues of gestational rats were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis, immunohistochemistry and western blotting. The associations between miR-27a and TLR4 were analyzed, and the regulatory effect of miR-27a on TLR4 was detected via a luciferase reporter gene assay, western blotting and RT-qPCR in vivo and in vitro. In addition, the present study demonstrated that miR-27a suppressed the expression of TLR4 by binding to the 3′UTR of TLR4. The overexpression of miR-27a downregulated the expression of TLR4, which in turn inhibited the inflammation, cell adhesion and cell death in IRI. Therefore, miR-27a inhibited inflammation in IRI by decreasing the expression of TLR4.