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Published on: October 19, 2013
Spatial and temporal expression of SP-B and TGF-β1 in hyperoxia-induced neonatal rat lung injury
Dongyun Liu1, Yingzi Liu2, Liping Dou3
1Department of Neonatal Intensive Care Unit, The Affiliated Hospital of Qingdao University Qingdao, P. R. China.
Insights
This study shows that surfactant protein-B (SP-B) and transforming growth factor-beta (TGF-β) are highly expressed in infant lung injury models. These factors increase in lung tissue and lavage fluid after 3 days of hyperoxia exposure.
Area of Science:
- Pulmonary Medicine
- Neonatology
- Developmental Biology
Background:
- Bronchopulmonary dysplasia (BPD) is a serious complication of extreme prematurity.
- Hyperoxia inhalation is a known cause of BPD.
- Surfactant protein-B (SP-B) and transforming growth factor-beta (TGF-β) are implicated in lung development.
Purpose of the Study:
- To investigate the spatial and temporal expression patterns of SP-B and TGF-β.
- To analyze their role in an animal model of BPD induced by hyperoxia.
Main Methods:
- Newborn Sprague-Dawley rats were exposed to hyperoxia to model BPD.
- Levels of SP-B, TGF-β, MDA, and TAOC were measured.
- MAPK and PI3K/AKT pathway activations were monitored in lung tissues.
Main Results:
- Hyperoxia induced body weight loss and impaired alveolar development in rats.
- SP-B and TGF-β mRNA and protein levels increased significantly by day 3 of hyperoxia.
- Oxidative stress markers (MDA increased, TAOC decreased) and altered signaling pathways (p38 activated, PI3K/AKT deactivated) were observed.
Conclusions:
- SP-B and TGF-β are upregulated in lung tissue and bronchoalveolar lavage fluid during hyperoxia-induced BPD.
- These changes are evident as early as 3 days after hyperoxia exposure.
- Findings suggest SP-B and TGF-β play a role in the pathogenesis of BPD.
Objective:
Bronchopulmonary dysplasia (BPD) is a severe complication of extreme prematurity that can be caused by hyperoxia inhalation. SP-B and TGF-β have been reported to be implicated in the development of lung. This study aimed to reveal the spatial and temporal expression patterns of these two factors in an animal model of BPD.
Methods:
Newborn Sprague-Dawley (SD) rats were subjected to hyperoxia conditions to establish an animal model of BPD. The levels of SP-B, TGF-β, MDA and TAOC, as well as the activations of MAPK and PI3K/AKT pathways in lung tissues were monitored during newborn rats prolonged exposure to hyperoxia.
Results:
We found that hyperoxia exposure significantly induced body weight loss of SD rats. H&E staining for morphometric analyses revealed that hyperoxia arrested alveolar development or loss of alveoli, with fewer and dysmorphic capillaries. mRNA and protein levels of SP-B and TGF-β were high expressed in hyperoxic lung tissues. The concentrations of SP-B and TGF-β in bronchoalveolar lavage fluid were also increased. All these increases begin at the 3th day of hyperoxia exposure. MDA content was increased while TAOC content was decreased in response to hyperoxia. Furthermore, hyperoxia activated p38, and deactivated PI3K and AKT expression.
Conclusion:
Our research demonstrated that SP-B and TGF-β1 were highly expressed in three levels: mRNA and protein levels in lung tissues, and the release of SP-B and TGF-β1 in bronchoalveolar lavage fluid, beginning at the 3th day of hyperoxia exposure.
