Clinical Diagnostic Value of miR-142-3p in Pediatric Acute Respiratory Distress Syndromes and Its Effects on Human Lung Epithelial Cells

Pediatric acute respiratory distress syndrome (PARDS) is a major cause of morbidity and mortality in critically ill children. microRNAs (miRNAs) were discovered to be involved in regulating the progression of numerous disorders, including PARDS. We aim to explore the diagnostic value and relevant mechanisms of miR-142-3p in PARDS. Real-time quantitative PCR (RT-qPCR) was used to detect the levels of miR-142-3p and myristoylated-alanine rich C-kinase substrate (MARCKS) in the serum of PARDS patients or in A549 cells. Receiver operating characteristic (ROC) curve analysis predicted the diagnostic value of miR-142-3p for PARDS. The proliferation, apoptosis and inflammatory factor concentrations in lipopolysaccharide (LPS)-induced A549 cells were measured using the Cell Counting Kit-8 (CCK-8) assay, flow cytometry and Enzyme-Linked Immunosorbent Assay (ELISA), respectively. We found that the content of miR-142-3p was markedly elevated in PARDS group and positively correlated with disease severity. It had good diagnostic ability for PARDS. Moreover, miR-142-3p and pro-inflammatory factors were remarkably positively correlated. In vitro, a cell model was constructed by inducing A549 cells with LPS. Cell proliferation was repressed while apoptosis and inflammation were facilitated in LPS-induced A549 cells. Up-regulated miR-142-3p enhanced apoptosis and inflammatory factor secretion while suppressed proliferation. Down-regulated miR-142-3p facilitated proliferation while repressed apoptosis and inflammatory factor secretion. Furthermore, MARCKS was a target gene of miR-142-3p and down-regulated in cell model. miR-142-3p may be a novel diagnostic marker for PARDS. In LPS-induced A549 cells, miR-142-3p repressed cell proliferation and facilitated apoptosis and inflammatory responses via modulating MARCKS.