ArticleScientific reports2020
S-endoglin expression is induced in hyperoxia and contributes to altered pulmonary angiogenesis in bronchopulmonary dysplasia development.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Caffeine Protects Against Hyperoxia-Induced Structural Lung Injury and Restores Alveolar Development in Neonatal Rats.Antioxidants (Basel, Switzerland) · 2025Article
- Glyceraldehyde 3-Phosphate Dehydrogenase and Galectin fromAnimals : an open access journal from MDPI · 2025Article
- Research progress of microvascular development in bronchopulmonary dysplasia.Pediatric investigation · 2024Review
- Association of cord blood Ang-1 and sCD105 levels with bronchopulmonary dysplasia in preterm infants.BMC pediatrics · 2024Article
- Post-translational modifications and bronchopulmonary dysplasia.Frontiers in pediatrics · 2024Review
- Lung epithelial-endothelial-mesenchymal signaling network with hepatocyte growth factor as a hub is involved in bronchopulmonary dysplasia.Frontiers in cell and developmental biology · 2024Review
- Sex-biased TGFβ signalling in pulmonary arterial hypertension.Cardiovascular research · 2023Review
- The role of rhIGF-1/BP3 in the prevention of pulmonary hypertension in bronchopulmonary dysplasia and its underlying mechanism.BMC pulmonary medicine · 2023Article
- CircRNA, lncRNA, and mRNA profiles of umbilical cord blood exosomes from preterm newborns showing bronchopulmonary dysplasia.European journal of pediatrics · 2022Article
- Perinatal Hyperoxia and Developmental Consequences on the Lung-Brain Axis.Oxidative medicine and cellular longevity · 2022Review
- TGF-β superfamily co-receptors in cancer.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Review
- BMP Receptor Inhibition Enhances Tissue Repair in Endoglin Heterozygous Mice.International journal of molecular sciences · 2021Article
- Hyperoxia and Lungs: What We Have Learned From Animal Models.Frontiers in medicine · 2021Review
- Alternative splicing in endothelial cells: novel therapeutic opportunities in cancer angiogenesis.Journal of experimental & clinical cancer research : CR · 2020Review
- Endothelial to mesenchymal transition during neonatal hyperoxia-induced pulmonary hypertension.The Journal of pathology · 2020Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Altered pulmonary angiogenesis contributes to disrupted alveolarization, which is the main characteristic of bronchopulmonary dysplasia (BPD). Transforming growth factor β (TGFβ) plays an important role during lung vascular development, and recent studies have demonstrated that endoglin is engaged in the modulation of TGFβ downstream signalling. Although there are two different isoforms of endoglin, L- and S-endoglin, little is known about the effect of S-endoglin in developing lungs. We analysed the expression of both L- and S-endoglin in the lung vasculature and its contribution to TGFβ-activin-like kinase (ALK)-Smad signalling with respect to BPD development. Hyperoxia impaired pulmonary angiogenesis accompanied by alveolar simplification in neonatal mouse lungs. S-endoglin, phosphorylated Smad2/3 and connective tissue growth factor levels were significantly increased in hyperoxia-exposed mice, while L-endoglin, phosphor-Smad1/5 and platelet-endothelial cell adhesion molecule-1 levels were significantly decreased. Hyperoxia suppressed the tubular growth of human pulmonary microvascular endothelial cells (ECs), and the selective inhibition of ALK5 signalling restored tubular growth. These results indicate that hyperoxia alters the balance in two isoforms of endoglin towards increased S-endoglin and that S-endoglin attenuates TGFβ-ALK1-Smad1/5 signalling but stimulates TGFβ-ALK5-Smad2/3 signalling in pulmonary ECs, which may lead to impaired pulmonary angiogenesis in developing lungs.
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