ArticleRespiratory research2023
Time-resolved transcriptomic profiling of the developing rabbit's lungs: impact of premature birth and implications for modelling bronchopulmonary dysplasia.
Article in Respiratory research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- Functional Dissection of TP63 Dual-Promoter Regulatory Elements Reveals Context-Dependent Responsiveness to FOXA2, NKX2-1, SOX9, and TP63-Related Inputs.Current issues in molecular biology · 2026Article
- A Premature Rabbit Kitten Model for Evaluation of Bronchopulmonary Dysplasia Therapies Reproduces Myeloperoxidase-Associated Pathology and Therapeutic Responses.International journal of molecular sciences · 2026Article
- Hyperoxia-induced lung microvascular injury is mediated by endothelial cell-derived WNT5A.Journal of thoracic disease · 2026Article
- Label-free optical fingerprints of hyperoxia-induced lung alterations in preterm rabbits.Respiratory research · 2026Article
- Investigating mitophagy mechanisms in bronchopulmonary dysplasia through bioinformatics.Pediatric research · 2026Article
- Identification of proteome-wide and functional analysis of lysine crotonylation in multiple organs of the human fetus.Proteome science · 2025Article
- Single, double, and triple-hit strategies to establish a long-term premature rabbit model of bronchopulmonary dysplasia.Respiratory research · 2025Article
- Longitudinal transcriptomic analysis of the hyperoxia-exposed preterm rabbit as a model of BPD.Frontiers in pediatrics · 2025Article
- Research progress of microvascular development in bronchopulmonary dysplasia.Pediatric investigation · 2024Review
- Association of Fetal Lung Development Disorders with Adult Diseases: A Comprehensive Review.Journal of personalized medicine · 2024Review
- A predictive model for preterm infants with bronchopulmonary dysplasia based on ferroptosis-related lncRNAs.BMC pulmonary medicine · 2023Article
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Authors and funding
21 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPremature birth, perinatal inflammation, and life-saving therapies such as postnatal oxygen and mechanical ventilation are strongly associated with the development of bronchopulmonary dysplasia (BPD); these risk factors, alone or combined, cause lung inflammation and alter programmed molecular patterns of normal lung development. The current knowledge on the molecular regulation of lung development mainly derives from mechanistic studies conducted in newborn rodents exposed to postnatal hyperoxia, which have been proven useful but have some limitations.
methodsHere, we used the rabbit model of BPD as a cost-effective alternative model that mirrors human lung development and, in addition, enables investigating the impact of premature birth per se on the pathophysiology of BPD without further perinatal insults (e.g., hyperoxia, LPS-induced inflammation). First, we characterized the rabbit's normal lung development along the distinct stages (i.e., pseudoglandular, canalicular, saccular, and alveolar phases) using histological, transcriptomic and proteomic analyses. Then, the impact of premature birth was investigated, comparing the sequential transcriptomic profiles of preterm rabbits obtained at different time intervals during their first week of postnatal life with those from age-matched term pups.
resultsHistological findings showed stage-specific morphological features of the developing rabbit's lung and validated the selected time intervals for the transcriptomic profiling. Cell cycle and embryo development, oxidative phosphorylation, and WNT signaling, among others, showed high gene expression in the pseudoglandular phase. Autophagy, epithelial morphogenesis, response to transforming growth factor β, angiogenesis, epithelium/endothelial cells development, and epithelium/endothelial cells migration pathways appeared upregulated from the 28th day of gestation (early saccular phase), which represents the starting point of the premature rabbit model. Premature birth caused a significant dysregulation of the inflammatory response. TNF-responsive, NF-κB regulated genes were significantly upregulated at premature delivery and triggered downstream inflammatory pathways such as leukocyte activation and cytokine signaling, which persisted upregulated during the first week of life. Preterm birth also dysregulated relevant pathways for normal lung development, such as blood vessel morphogenesis and epithelial-mesenchymal transition.
conclusionThese findings establish the 28-day gestation premature rabbit as a suitable model for mechanistic and pharmacological studies in the context of BPD.
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