Background: Previous studies have showed that lncRNA MCM3AP-AS1 and miR-223 play opposite roles in LPS-induced inflammation, which contributes to the progression of sepsis. This study was therefore carried out to analyze the interactions between MCM3AP-AS1 and miR-223 in sepsis.
Methods: Plasma samples were obtained from 62 sepsis patients and 62 healthy controls. Expression of MCM3AP-AS1, miR-223 precursor and mature miR-223 in plasma samples was determined by RT-qPCR. In human bronchial epithelial cells (HBEpCs), the interaction between MCM3AP-AS1 and miR-223 was analyzed by overexpression experiments. Cell apoptosis assay was analyzed by cell apoptosis assay.
Results: We found that MCM3AP-AS1 was upregulated in sepsis, while miR-223 was downregulated in sepsis. MCM3AP-AS1 and mature miR-223 were inversely correlated, while MCM3AP-AS1 and miR-223 precursor were not. In HBEpCs, LPS treatment resulted in the upregulation of MCM3AP-AS1 and downregulation of miR-223. In HBEpCs, MCM3AP-AS1 overexpression downregulated mature miR-223 but failed to affect miR-223 precursor. In addition, MCM3AP-AS1 overexpression reduced the inhibitory effects of miR-223 on LPS-induced apoptosis of HBEpCs.
Conclusions: LncRNA MCM3AP-AS1 is upregulated in sepsis and may suppress the maturation of miR-223 to promote LPS-induced lung cells.