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@ARTICLE{Storti:274372,
      author       = {M. Storti and M. L. Faietti and X. Murgia and C. Catozzi
                      and I. Minato and D. Tatoni and S. Cantarella$^*$ and F.
                      Ravanetti and L. Ragionieri and R. Ciccimarra and M. Zoboli
                      and M. Vilanova and E. Sánchez-Jiménez and M. Gay and M.
                      Vilaseca and G. Villetti and B. Pioselli and F. Salomone and
                      S. Ottonello and B. Montanini and F. Ricci},
      title        = {{T}ime-resolved transcriptomic profiling of the developing
                      rabbit's lungs: impact of premature birth and implications
                      for modelling bronchopulmonary dysplasia.},
      journal      = {Respiratory research},
      volume       = {24},
      number       = {1},
      issn         = {1465-9921},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DKFZ-2023-00574},
      pages        = {80},
      year         = {2023},
      abstract     = {Premature 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.Here, 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.Histological 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.These
                      findings establish the 28-day gestation premature rabbit as
                      a suitable model for mechanistic and pharmacological studies
                      in the context of BPD.},
      keywords     = {Animals / Pregnancy / Female / Rabbits / Infant, Newborn /
                      Humans / Bronchopulmonary Dysplasia: genetics /
                      Bronchopulmonary Dysplasia: pathology / Premature Birth:
                      metabolism / Hyperoxia: metabolism / Transcriptome /
                      Endothelial Cells: metabolism / Proteomics / Animals,
                      Newborn / Lung: metabolism / Inflammation: metabolism /
                      Bronchopulmonary dysplasia (Other) / Lung development
                      (Other) / Premature birth (Other) / Proteomics (Other) /
                      Transcriptomics (Other)},
      cin          = {B150},
      ddc          = {610},
      cid          = {I:(DE-He78)B150-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36922832},
      pmc          = {pmc:PMC10015812},
      doi          = {10.1186/s12931-023-02380-y},
      url          = {https://inrepo02.dkfz.de/record/274372},
}