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Epithelial-mesenchymal transitions in bronchopulmonary dysplasia of newborn rats
Haiping Yang1, Jianhua Fu, Xindong Xue
1Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, China.
Insights
Epithelial-mesenchymal transition (EMT) in alveolar epithelial cells contributes to bronchopulmonary dysplasia (BPD) in newborn rats. This process impairs lung development, highlighting a potential therapeutic target for BPD.
Area of Science:
- Neonatal pathology
- Pulmonary research
- Cellular biology
Background:
- Bronchopulmonary dysplasia (BPD) poses significant risks to premature infants, with unclear underlying mechanisms.
- Epithelial-mesenchymal transition (EMT) in lung epithelial cells is a potential contributor to BPD pathogenesis.
Purpose of the Study:
- To investigate the occurrence and role of EMT in a newborn rat model of hyperoxia-induced BPD.
Main Methods:
- Newborn rats were exposed to hyperoxia.
- Lung tissue and alveolar epithelial type II (AT2) cells were analyzed for pathological changes, alveolar development, and EMT markers (SPC, α-SMA, E-cadherin, N-cadherin).
Main Results:
- Hyperoxia-induced BPD in rats showed attenuated alveolar development from Day 7.
- AT2 cells exhibited ultrastructural changes and co-expression of SPC and α-SMA, indicative of EMT.
- A shift from E-cadherin to N-cadherin expression was observed in BPD lung tissue and AT2 cells.
Conclusions:
- EMT of AT2 cells occurs in this hyperoxia-induced BPD model.
- EMT contributes to attenuated alveolar development, with AT2 cells differentiating into myofibroblasts.
Background:
Bronchopulmonary dysplasia (BPD) is a major threat to the health of premature infants yet its pathogenesis is not fully understood. Epithelial-mesenchymal transition (EMT) of lung epithelial cells may lead to BPD.
Objective:
To investigate the potential occurrence of EMT in a newborn rat model of BPD.
Methods:
Newborn rats were exposed to a hyperoxic environment within 12 hr of birth. Lung tissue and isolated alveolar epithelial type II cells (AT2 cells) were collected on Days 1, 3, 7, 14, and 21 after hyperoxic exposure. Pathological changes in lung tissue, alveolar development, ultrastructural changes in AT2 cells, co-expression of surfactant associated surfactant protein C (SPC), and α-smooth muscle actin (α-SMA) were investigated. The relative expression of SPC, α-SMA, E-cadherin, and N-cadherin were investigated in lung tissue and isolated AT2 cells.
Results:
In lung tissue, alveolar development was attenuated from Day 7 onwards in the BPD model group; co-expression of SPC and α-SMA and ultrastructural changes typical of EMT were observed in AT2 cells from rats in the BPD group. SPC and α-SMA expression levels were higher in tissue samples from the BPD group than in control samples. Beginning on Day 7, evidence of a switch from E-cadherin to N-cadherin expression was observed in BPD lung tissue sample and in isolated AT2 cells.
Conclusion:
EMT of AT2 cells occurred in the hyperoxia-induced newborn rat BPD model and resulted in attenuated alveolar development as a portion of the myofibroblasts accumulated in the lung originated from AT2 cells via EMT.
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