ArticlePediatric research2019
Hyperoxia causes miR199a-5p-mediated injury in the developing lung.
Article in Pediatric research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Neonatal kidney injury in the hyperoxia-induced bronchopulmonary dysplasia mouse models: effect on morphology and biomarkers.Pediatric research · 2026Article
- [Expression and regulatory mechanism of miR-34a in neonatal rat model of bron-chopulmonary dysplasia induced by hyperoxia].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2025Article
- Article
- The vascular phenotype of BPD: new basic science insights-new precision medicine approaches.Pediatric research · 2024Review
- miRNA Signatures in Bronchopulmonary Dysplasia: Implications for Biomarkers, Pathogenesis, and Therapeutic Options.Frontiers in bioscience (Landmark edition) · 2024Review
- Article
- Oxygen toxicity: cellular mechanisms in normobaric hyperoxia.Cell biology and toxicology · 2023Review
- Association of immune cell recruitment and BPD development.Molecular and cellular pediatrics · 2022Review
- Adiponectin ameliorates hyperoxia-induced lung endothelial dysfunction and promotes angiogenesis in neonatal mice.Pediatric research · 2022Article
- Patho-mechanisms of the origins of bronchopulmonary dysplasia.Molecular and cellular pediatrics · 2021Review
- Tracheal aspirate transcriptomic and miRNA signatures of extreme premature birth with bronchopulmonary dysplasia.Journal of perinatology : official journal of the California Perinatal Association · 2021Article
- Signaling Pathways Involved in the Development of Bronchopulmonary Dysplasia and Pulmonary Hypertension.Children (Basel, Switzerland) · 2020Review
- Role of extracellular vesicles in cell-cell communication and inflammation following exposure to pulmonary toxicants.Cytokine & growth factor reviews · 2020Review
- Recent advances in understanding and management of bronchopulmonary dysplasia.F1000Research · 2020Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHyperoxia-induced acute lung injury (HALI) is characterized by increased permeability and infiltration of inflammatory cells, impairment of alveolar development, and compromised lung function. Recent evidence has determined that microRNAs (miRs) are implicated in hyperoxia-induced lung injury, including bronchopulmonary dysplasia (BPD). However, the expression profile and functional role of miR199a-5p in developing lungs have not been reported.
methodsThe present study was undertaken to explore the role of miR199a-5p in developing mice lungs and human neonates. We exposed neonatal mice for 7 days, mouse lung epithelial cells (MLE12), mouse lung endothelial cells (MLECs), and macrophages (RAW246.7), to hyperoxia at different time points.
resultsOur results demonstrated enhanced miR199a-5p expression in hyperoxia-exposed mice lungs and cells, as well as in tracheal aspirates of infants developing BPD, with significant reduction in the expression of its target, caveolin-1. Next, we observed that miR199a-5p-mimic worsens HALI as evidenced by increased inflammatory cells, cytokines, and lung vascular markers. Conversely, miR199a-5p-inhibitor treatment attenuated HALI.
conclusionThus, our findings suggest that miR199a-5p is a potential target for attenuating HALI pathophysiology in the developing lung. Moreover, miR199a-5p-inhibitor could be part of a novel therapeutic strategy for improving BPD in preterm neonates.
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