ArticleThe American journal of pathology2016
Initial Suppression of Transforming Growth Factor-β Signaling and Loss of TGFBI Causes Early Alveolar Structural Defects Resulting in Bronchopulmonary Dysplasia.
Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 59 citations in OpenAlex.
- Pro-inflammatory and matricellular protein expression patterns associated with bronchopulmonary dysplasia severity.Pediatric research · 2026Article
- The Inflammatory Nexus of Bronchopulmonary Dysplasia: From Molecular Pathways to Precision Therapeutics.Mediators of inflammation · 2026Review
- DNA methylation and hydroxymethylation combined with transcriptional profiling identify key regulators of hyperoxia-induced bronchopulmonary dysplasia.Clinical epigenetics · 2025Article
- Novel Porcine Model Reveals Two Distinct LGR5 Cell Types during Lung Development and Homeostasis.American journal of respiratory cell and molecular biology · 2025Article
- Endothelial Cpt1a Inhibits Neonatal Hyperoxia-Induced Pulmonary Vascular Remodeling by Repressing Endothelial-Mesenchymal Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Impaired myofibroblast proliferation is a central feature of pathologic post-natal alveolar simplification.eLife · 2024Article
- Impaired Myofibroblast Proliferation is a Central Feature of Pathologic Post-Natal Alveolar Simplification.bioRxiv : the preprint server for biology · 2024Article
- TGFBI promotes proliferation and epithelial-mesenchymal transition in renal cell carcinoma through PI3K/AKT/mTOR/HIF-1α pathway.Cancer cell international · 2024Article
- Enter the Matrix: Fibroblast-immune cell interactions shape extracellular matrix deposition in health and disease.F1000Research · 2024Review
- New Insights in the Pathology of Chronic Thromboembolic Pulmonary Hypertension.JACC. Basic to translational science · 2024Article
- Opposing roles for TGFβ- and BMP-signaling during nascent alveolar differentiation in the developing human lung.NPJ Regenerative medicine · 2023Article
- Cord blood transforming growth factor-β-induced as predictive biomarker of retinopathy of prematurity in preterm infants.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2023Article
- Comparative Analysis of Epididymis Cauda of Yak before and after Sexual Maturity.Animals : an open access journal from MDPI · 2023Article
- Time-resolved transcriptomic profiling of the developing rabbit's lungs: impact of premature birth and implications for modelling bronchopulmonary dysplasia.Respiratory research · 2023Article
- Complex roles of TGF-β signaling pathways in lung development and bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- Role of Postnatal Corticosteroids in the Treatment or Prevention of Bronchopulmonary Dysplasia.Sisli Etfal Hastanesi tip bulteni · 2023Review
- Proteomic analysis identifies a signature of disease severity in the plasma of COVID-19 pneumonia patients associated to neutrophil, platelet and complement activation.Clinical proteomics · 2022Article
- Maladaptive functional changes in alveolar fibroblasts due to perinatal hyperoxia impair epithelial differentiation.JCI insight · 2022Article
- Patho-mechanisms of the origins of bronchopulmonary dysplasia.Molecular and cellular pediatrics · 2021Review
- miR-145 transgenic mice develop cardiopulmonary complications leading to postnatal death.Physiological reports · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Septation of the gas-exchange saccules of the morphologically immature mouse lung requires regulated timing, spatial direction, and dosage of transforming growth factor (TGF)-β signaling. We found that neonatal hyperoxia acutely initially diminished saccular TGF-β signaling coincident with alveolar simplification. However, sustained hyperoxia resulted in a biphasic response and subsequent up-regulation of TGF-β signaling, ultimately resulting in bronchopulmonary dysplasia. Significantly, we found that the TGF-β-induced matricellular protein (TGFBI) was similarly biphasically altered in response to hyperoxia. Moreover, genetic ablation revealed that TGFBI was required for normal alveolar structure and function. Although the phenotype was not neonatal lethal, Tgfbi-deficient lungs were morphologically abnormal. Mutant septal tips were stunted, lacked elastin-positive tips, exhibited reduced proliferation, and contained abnormally persistent alveolar α-smooth muscle actin myofibroblasts. In addition, Tgfbi-deficient lungs misexpressed TGF-β-responsive follistatin and serpine 1, and transiently suppressed myofibroblast platelet-derived growth factor α differentiation marker. Finally, despite normal lung volume, Tgfbi-null lungs displayed diminished elastic recoil and gas exchange efficiency. Combined, these data demonstrate that initial suppression of the TGF-β signaling apparatus, as well as loss of key TGF-β effectors (like TGFBI), underlies early alveolar structural defects, as well as long-lasting functional deficits routinely observed in chronic lung disease of infancy patients. These studies underline the complex (and often contradictory) role of TGF-β and indicate a need to design studies to associate alterations with initial appearance of phenotypical changes suggestive of bronchopulmonary dysplasia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.