MiR‐545‐3p: A Potential Diagnostic and Prognostic Biomarker for NRDS and Regulator of Inflammation via TNFSF13B
Zhijuan Shi, Yanmei He, Xukai ShiABSTRACT
Background
Neonatal respiratory distress syndrome (NRDS) is a severe respiratory disease prevalent in preterm neonates. Pulmonary inflammation is an important factor that exacerbates disease severity and prolongs the clinical course of NRDS.
Aim
This study investigated the potential diagnostic and prognostic value of miR‐545‐3p in NRDS and its regulatory effect on cell inflammation by targeting TNFSF13B , providing a preliminary experimental basis for NRDS research.
Methods
A total of 300 preterm neonates were enrolled, including 150 with NRDS and 150 non‐NRDS controls. MiR‐545‐3p and TNFSF13B expression in plasma was detected by RT‐qPCR. The targeting relationship between miR‐545‐3p and TNFSF13B was validated using bioinformatics analysis and a dual‐luciferase reporter assay. LPS‐treated A549 cells served as an inflammatory epithelial injury model, with cell viability and inflammatory factor levels assessed by CCK‐8 and ELISA assays, respectively.
Results
MiR‐545‐3p exhibited significant downregulation in neonates with NRDS, and its close correlation with LUS and SNAPPE‐II scores suggests diagnostic and prognostic potential. ROC and logistic analyses evaluated its diagnostic value (AUC = 0.748; OR = 0.139, 95% CI: 0.083–0.233, p < 0.001) and prognostic value for non‐survival (AUC = 0.792; OR = 0.173, 95% CI: 0.067–0.446, p < 0.001). TNFSF13B was identified as the direct target. The inhibitory effects of miR‐545‐3p on LPS‐induced reduction of A549 cell viability and pro‐inflammatory factor secretion were reversed by TNFSF13B overexpression.
Conclusions
MiR‐545‐3p may serve as a potential auxiliary molecular marker for the diagnosis and prognostic evaluation of NRDS. The miR‐545‐3p/ TNFSF13B axis may be involved in regulating pulmonary inflammation in NRDS.