ArticleJournal of lung, pulmonary & respiratory research2019
Activation of mas restores hyperoxia-induced loss of lung epithelial barrier function through inhibition of apoptosis.
Article in Journal of lung, pulmonary & respiratory research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Review
- Alpha-1 antitrypsin limits neutrophil extracellular trap disruption of airway epithelial barrier function.Frontiers in immunology · 2022Article
- Claudin-18 expression under hyperoxia in neonatal lungs of bronchopulmonary dysplasia model rats.Frontiers in pediatrics · 2022Article
- Article
- [A review on the effect of Claudin-18 on bronchopulmonary dysplasia in preterm infants].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2021Review
- Regulation of ACE-2 enzyme by hyperoxia in lung epithelial cells by post-translational modification.Journal of lung, pulmonary & respiratory research · 2021Article
- Angiotensin Converting Enzyme-2 (ACE-2) role in disease and future in research.Journal of lung, pulmonary & respiratory research · 2021Article
- Mas Receptor Agonist AVE0991 increases surfactant protein expression under hyperoxic conditions in human lung epithelial cells.Journal of lung, pulmonary & respiratory research · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNeonatal therapy with a high concentration of oxygen (hyperoxia) is a known cause of bronchopulmonary dysplasia (BPD). BPD is characterized by increased pulmonary permeability and diffuse infiltration of various inflammatory cells. Disruption of the epithelial barrier may lead to altered pulmonary permeability and airways fluid accumulation. Mas receptor is a component of the renin angiotensin system and is the receptor for the protective endogenous peptide angiotensin 1-7. The activation of the Mas receptor was previously shown to have protective pulmonary responses. However, the effect of Mas receptor activation on epithelial barrier integrity has not been tested.
objectiveTo determine the effects of hyperoxia with or without Mas receptor activation on epithelial cell barrier integrity. DESIGN/
methodsHuman epithelial cell line A549 was cultured on transwell polycarbonate porous membrane to confluence and treated with 95% oxygen (hyperoxia) for 72 hours with or without the Mas receptor agonist (AVE0991), or the apoptotic inhibitors Z-VAD-FMK or aurintricarboxylic acid. The cells were then challenged with Rhodamine labeled bovine serum albumin (Rh-BSA) on one side of the membrane. Fluorescent quantitation of Rh-BSA (albumin flux) was performed on the media in the other side of the membrane 3 hours later and was compared with 21% oxygen (Normoxia) control group. A549 cells were also cultured with or without AVE0991 in hyperoxia or normoxia and used for nuclear fragmentation apoptosis assay using propidium iodide staining.
resultsHyperoxia induced an increase in albumin flux that was significantly prevented by AVE0991 treatment and by the apoptosis inhibitors. AVE0991 also significantly decreased the hyperoxia-induced nuclear fragmentation.
conclusionThese results suggest that hyperoxia causes a disruption in the epithelial barrier integrity, and that this disruption is inhibited by the Mas receptor agonist AVE0991 through inhibition of epithelial apoptosis. These results reveal a novel potential drug for BPD and pulmonary edema treatment.
Indexed as
Identifiers
32632378PMC7338093W3040779280What Socratic holds
Registered trials
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