Screening for biomarkers of bronchopulmonary dysplasia: a bioinformatics analysis

Bronchopulmonary dysplasia (BPD) is a common chronic respiratory disease in preterm infants, and its incidence has gradually increased with advances in medical technology. BPD is associated with multiple complications, significantly impacting the quality of life of affected infants and imposing substantial economic burdens on families and society. Currently, the molecular mechanisms of BPD are not fully understood, and effective treatments are lacking. MicroRNAs (miRNAs), as important gene regulatory molecules, play a critical role in lung development and BPD. This study aims to investigate the potential role of miRNAs in BPD, with a particular focus on miR-9-5p and guanosine triphosphate cyclohydrolase 1 (GCH1).

Differential expression analysis of genes and miRNAs was conducted using the Gene Expression Omnibus (GEO) database. A hyperoxia-induced injury cell model was constructed to examine the expression of miR-9-5p. Target genes of miR-9-5p were predicted using online databases, followed by functional and protein interaction network analyses. In addition, cell culture, real-time quantitative polymerase chain reaction (RT-qPCR), western blotting, reactive oxygen species (ROS) level detection, malondialdehyde (MDA) assay, and Fe²⁺ detection experiments were performed.

In the GSE108755 dataset, miR-9-5p was found to be upregulated in the blood of infants with BPD. In the hyperoxia-induced injury cell model, miR-9-5p expression was significantly increased. GCH1 was identified as a target gene through intersection with ferroptosis regulatory gene sets. In the cell model, GCH1 expression was markedly downregulated, while ROS, MDA, and Fe²⁺ levels were significantly elevated.

This study provides new insights into the molecular mechanisms of BPD, suggesting that miR-9-5p and GCH1 may serve as potential therapeutic targets for BPD. The findings contribute to a deeper understanding of the molecular basis of BPD, providing theoretical and experimental support for its diagnosis and treatment strategies. Future research will further explore the regulatory relationship between miR-9-5p and GCH1 and their roles in animal models, cell models, and clinical patients.