ArticleInternational journal of clinical and experimental pathology2018
Spatial and temporal expression of SP-B and TGF-β1 in hyperoxia-induced neonatal rat lung injury.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Complex roles of TGF-β signaling pathways in lung development and bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- Weighted Gene Co-expression Network Analysis of Key Biomarkers Associated With Bronchopulmonary Dysplasia.Frontiers in genetics · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveBronchopulmonary 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.
methodsNewborn 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.
resultsWe 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.
conclusionOur 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.
Indexed as
Identifiers
31938105PMC6957977W3012086122What OpenQuestion holds
Registered trials
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