ArticleAmerican journal of respiratory and critical care medicine2011
Inhibiting lung elastase activity enables lung growth in mechanically ventilated newborn mice.
Article in American journal of respiratory and critical care medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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44 citing papers in PubMed, 77 citations in OpenAlex.
- Respiratory outcomes of the surfactant positive pressure and oximetry randomized trial (SUPPORT).The Journal of pediatrics · 2014Trial
- The evolving pathophysiology of bronchopulmonary dysplasia.Physiological reviews · 2026Review
- Targeting IL6-Edn1-FoxO1 axis enables lung growth in mechanically ventilated newborn mice.The European respiratory journal · 2025Article
- Th1 differentiation and function are inhibited in neonates following human metapneumovirus infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Hemodynamic Changes in the Transition Period in the Preterm and Term Infant: Basic Concepts.Turkish archives of pediatrics · 2025Article
- Prenatal vitamin D supplementation mitigates inflammation-related alveolar remodeling in neonatal mice.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Complex roles of TGF-β signaling pathways in lung development and bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- Article
- Association of immune cell recruitment and BPD development.Molecular and cellular pediatrics · 2022Review
- When inflammation meets lung development-an update on the pathogenesis of bronchopulmonary dysplasia.Molecular and cellular pediatrics · 2022Review
- Lysyl oxidase regulation and protein aldehydes in the injured newborn lung.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Macrophage-derived IL-6 trans-signalling as a novel target in the pathogenesis of bronchopulmonary dysplasia.The European respiratory journal · 2022Article
- Patho-mechanisms of the origins of bronchopulmonary dysplasia.Molecular and cellular pediatrics · 2021Review
- Reduced neutrophil elastase inhibitor elafin and elevated transforming growth factor-βERJ open research · 2021Article
- Early Changes and Indicators Characterizing Lung Aging in Neonatal Chronic Lung Disease.Frontiers in medicine · 2021Review
- Use of Nasoil® via intranasal to control the harmful effects of Covid-19.Microbial pathogenesis · 2020Article
- IL-33-induced neutrophil extracellular traps degrade fibronectin in a murine model of bronchopulmonary dysplasia.Cell death discovery · 2020Article
- Mechanisms of Ventilator-induced Lung Injury: Is the Elafin in the Room?American journal of respiratory cell and molecular biology · 2018Article
- Elafin Treatment Rescues EGFR-Klf4 Signaling and Lung Cell Survival in Ventilated Newborn Mice.American journal of respiratory cell and molecular biology · 2018Article
- Interleukin-33 (IL-33) Increases Hyperoxia-Induced Bronchopulmonary Dysplasia in Newborn Mice by Regulation of Inflammatory Mediators.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
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11 authors at 3 institutions in 2 countries.
Funding
Abstract
rationaleMechanical ventilation with O₂-rich gas (MV-O₂) offers life-saving treatment for respiratory failure, but also promotes lung injury. We previously reported that MV-O2 of newborn mice increased lung elastase activity, causing elastin degradation and redistribution of elastic fibers from septal tips to alveolar walls. These changes were associated with transforming growth factor (TGF)-β activation and increased apoptosis leading to defective alveolarization and lung growth arrest, as seen in neonatal chronic lung disease.
objectivesTo determine if intratracheal treatment of newborn mice with the serine elastase inhibitor elafin would prevent MV-O₂-induced lung elastin degradation and the ensuing cascade of events causing lung growth arrest.
methodsFive-day-old mice were treated via tracheotomy with recombinant human elafin or vehicle (lactated-Ringer solution), followed by MV with 40% O₂ for 8-24 hours; control animals breathed 40% O₂ without MV. At study's end, lungs were harvested to assess key variables noted below. MEASUREMENTS AND MAIN
resultsMV-O₂ of vehicle-treated pups increased lung elastase and matrix metalloproteinase-9 activity when compared with unventilated control animals, causing elastin degradation (urine desmosine doubled), TGF-β activation (pSmad-2 tripled), and apoptosis (cleaved-caspase-3 increased 10-fold). Quantitative lung histology showed larger and fewer alveoli, greater inflammation, and scattered elastic fibers. Elafin blocked these MV-O₂-induced changes.
conclusionsIntratracheal elafin, by blocking lung protease activity, prevented MV-O₂-induced elastin degradation, TGF-β activation, apoptosis, and dispersion of matrix elastin, and attenuated lung structural abnormalities noted in vehicle-treated mice after 24 hours of MV-O₂. These findings suggest that elastin breakdown contributes to defective lung growth in response to MV-O₂ and might be targeted therapeutically to prevent MV-O₂-induced lung injury.
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