Long noncoding RNA MALAT1 can regulate proliferation and apoptosis of LPS-treated HK-2 cells via targeting miR-23a-3p through regulating ERK signaling

Abstract

IntroductionThe aim of the present study was to investigate the roles of long noncoding RNA (lncRNA) MALAT1 in the development of sepsis-induced acute kidney injury (septic AKI) and the underlying mechanism.Material and methodsThe levels of MALAT1 in the serum of the septic AKI patients and healthy subjects were compared, and the targeting relationship between MALAT1 and miR-23a-3p was analyzed. Moreover, the effects of MALAT1 and miR-23a-3p on the proliferation and apoptosis of LPS-treated HK-2 cells were analyzed. Finally, the roles of ERK signaling during this process were analyzed.ResultsWe found that MALAT1 was markedly increased in serum of the septic AKI patients and LPS-treated cells. In addition, overexpression of MALAT1 relieved the injury induced by LPS in RMCs. Moreover, miR-23-a-3p has been confirmed as a target of MALAT1. Meanwhile, we also found that MALAT1 siRNA can increase the proliferation and inhibit the apoptosis of LPS-treated HK-2 cells through activating ERK signaling, and knockdown of miR-23a-3p can partially block the anti-apoptotic effect of MALAT1 siRNA.ConclusionsWe report that MALAT1 can regulate the proliferation and apoptosis of LPS-treated HK-2 cells via targeting miR-23a-3p through regulating ERK signaling, suggesting that the MALAT1/miR-23a-3p axis could serve as a potential therapeutic target for the treatment of septic AKI.