MiR-629-5p May serve as a biomarker for pediatric acute respiratory distress syndrome and can regulate the inflammatory response.

ABSTRACT

OBJECTIVE: Circulating microRNAs (miRNAs) are associated with pediatric acute respiratory distress syndromes (PARDS). This study analyzed the clinical significance and potential mechanism of microRNA (miR)-629-5p in PARDS. METHODS: 82 children with PARDS and 82 controls were enrolled. Serum levels of miR-629-5p were measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and its diagnostic significance with respect to for PARDS in children was assessed by the receiver operating characteristic (ROC). Kaplan-Meier curve and multivariate Cox regression were utilized to examine the prognostic significance of miR-629-5p. An in vitro cell model was established using lipopolysaccharide (LPS)-induced alveolar epithelial cells A549. The cell proliferation, apoptosis, and inflammatory factors were assessed using cell counting kit-8 (CCK-8), flow cytometry, and enzyme-linked immunosorbent assay (ELISA). miR-629-5p target genes were identified in the database and validated using the dual-luciferase report assay. RESULTS: Serum miR-629-5p levels were significantly higher in children with PARDS than in controls (P < 0.05). miR-629-5p exhibited 86.6% sensitivity and 91.5% specificity in distinguishing children with PARDS. miR-629-5p was an independent risk factor for mortality, and high levels of miR-629-5p have a poor prognosis. LPS promoted apoptosis and overproduction of inflammatory factors in A549 and upregulated miR-629-5p expression (P < 0.05); however, they were partially reversed by the weakened miR-629-5p (P < 0.05). Syndecan-4 (SDC4) is a target of miR-629-5p. The inhibition of SDC4 induced by LPS can be alleviated through the reduction of miR-629-5p. CONCLUSION: miR-629-5p serves as a diagnostic biomarker for children with PARDS and it is associated with poor prognosis. Diminished miR-629-5p may alleviate PARDS by targeting SDC4 to suppress apoptosis and inflammation of alveolar epithelial cells.