Peptidome analysis of lung tissues from a hyperoxia‐induced bronchopulmonary dysplasia mouse model: Insights into the pathophysiological process of bronchopulmonary dysplasia
The aim of this study was to identify and compare the peptidomic profiles of lung tissues from neonatal mice with and without bronchopulmonary dysplasia (BPD). Hyperoxia was used to establish the BPD mouse model. Lung tissues obtained on postnatal day (PND) 9 were processed for analysis via histolog...
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Veröffentlicht in: | Journal of cellular physiology 2018-10, Vol.233 (10), p.7101-7112 |
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Sprache: | eng |
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Zusammenfassung: | The aim of this study was to identify and compare the peptidomic profiles of lung tissues from neonatal mice with and without bronchopulmonary dysplasia (BPD). Hyperoxia was used to establish the BPD mouse model. Lung tissues obtained on postnatal day (PND) 9 were processed for analysis via histological staining and label‐free liquid chromatography‐mass spectrometry (LC‐MS/MS). Histological analysis of the lung sections from the BPD group showed significant alveolar simplification and aberrant pulmonary vascularization. We identified 3,704 total peptides, of which 63 were differentially expressed in the lung tissues from the BPD group compared with those from the control group. Within this subset, 31 peptides were downregulated, and 32 peptides were upregulated. Bioinformatics analysis suggested several potential roles of the differentially expressed peptides in the pathophysiological process of BPD. In summary, this study highlights novel peptide candidates, and provides new insights for further understanding the molecular mechanism of BPD development.
Using label‐free LC‐MS/MS, we have identified and compared the peptidomic profiles of lung tissues from neonatal mice with or without hyperoxia‐induced BPD and observed significantly different expression patterns. These data provide new insights into the pathogenesis mechanism of BPD and may help us to discover novel markers to better predict and prevent BPD. |
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ISSN: | 0021-9541 1097-4652 |
DOI: | 10.1002/jcp.26633 |