Long noncoding RNA Mirt2 prohibits lipopolysaccharide-evoked HK-2 cell injury via modulation of microRNA-126.

Long noncoding RNA myocardial infarction-associated transcript 2 (lncRNA Mirt2) is a burgeoning lncRNA, its anti-inflammatory capacity has been testified. Nonetheless, the functions of Mirt2 in immunoglobulin A nephropathy are unexplored. We tried to impart the influences of Mirt2 in lipopolysaccharide (LPS)-evoked HK-2 cells damage. HK-2 cells were manipulated with 10 ng/ml LPS, next cell viability, apoptosis, reactive oxygen species (ROS) generation, pro-inflammatory factors and Mirt2 expression were evaluated. After pc-Mirt2 vector transfection, the aforementioned trials were performed. Meanwhile, real-time quantitative polymerase chain reaction (PCR) experiment was used to detect miR-126 expression. Subsequently, functions of miR-126 in LPS-treated HK-2 cells were further delved after transfection with miR-126 mimic. Western blot was used to evaluate NF-κB pathway. The data showed that LPS invoked HK-2 cells inflammatory damage via the suppression of cell viability and the acceleration of apoptosis, ROS level, and IL-1β and IL-6 secretion. LPS inhibited Mirt2 expression and overexpression of Mirt2 mitigated LPS-caused inflammatory damage in HK-2 cells. Additionally, overexpression of Mirt2 repressed miR-126 expression in LPS-stimulated cells. Meanwhile the anti-inflammatory effect of Mirt2 was inverted by upregulating miR-126 expression. Besides, overexpressed Mirt2 retarded LPS-activated NF-κB pathway via repressing miR-126. The research certified the anti-inflammatory impacts of Mirt2 on LPS-impaired HK-2 cells.