ArticleExperimental lung research2016
Prior hypoxia prevents downregulation of ACE-2 by hyperoxia in fetal human lung fibroblasts.
Article in Experimental lung research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Inhibition of SARS-CoV-2 spike S1-ACE2 binding interaction and downregulation of ACE2 gene expression by Malaysian stingless bee honey and its bioactive compound, stilbamidine (SDC).Molecular biology reports · 2026Article
- Review
- Alternative RAS in Various Hypoxic Conditions: From Myocardial Infarction to COVID-19.International journal of molecular sciences · 2021Review
- New perspectives on angiotensin-converting enzyme 2 and its related diseases.World journal of diabetes · 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
- The conundrum of using hyperoxia in COVID-19 treatment strategies: may intermittent therapeutic hyperoxia play a helpful role in the expression of the surface receptors ACE2 and Furin in lung tissue via triggering of HIF-1α?Intensive care medicine experimental · 2020Article
- Geographic components of SARS-CoV-2 expansion: a hypothesis.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Review
- Application of System Biology to Explore the Association of Neprilysin, Angiotensin-Converting Enzyme 2 (ACE2), and Carbonic Anhydrase (CA) in Pathogenesis of SARS-CoV-2.Biological procedures online · 2020Article
- Oxygen injury in neonates: which is worse? hyperoxia, hypoxia, or alternating hyperoxia/hypoxia.Journal of lung, pulmonary & respiratory research · 2020Article
- Article
- Activation of mas restores hyperoxia-induced loss of lung epithelial barrier function through inhibition of apoptosis.Journal of lung, pulmonary & respiratory research · 2019Article
- The renin angiotensin system in liver and lung: impact and therapeutic potential in organ fibrosis.Journal of lung, pulmonary & respiratory research · 2018Article
- Regulation of the angiotensin II-p22phox-reactive oxygen species signaling pathway, apoptosis and 8-oxoguanine-DNA glycosylase 1 retrieval in hyperoxia-induced lung injury and fibrosis in rats.Experimental and therapeutic medicine · 2017Article
- The unfolded protein response controls ER stress-induced apoptosis of lung epithelial cells through angiotensin generation.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Roles of the Angiotensin System in Neonatal Lung Injury and Disease.JSM atherosclerosis · 2016Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledPurpose/Aim of Study: The renin angiotensin system is involved in experimentally induced lung fibrosis. Angiotensin (ANG)-II is profibrotic. Angiotensin converting enzyme-2 (ACE-2) cleaves ANG-II and is thus protective. ACE-2 has recently been reported to be significantly decreased under hyperoxic conditions. Hyperoxia is linked to Bronchopulmonary Dysplasia and lung fibrosis. Fetal lung cells normally do not undergo fibrotic changes with physiologic hypoxemia. We hypothesized that hypoxia prior to hyperoxic exposure in fetal lung fibroblasts (IMR-90 cell line) might be protective by preventing ACE-2 downregulation. MATERIALS AND
methodsIMR-90 cells were exposed to hypoxia (1%O2/99%N2) followed by hyperoxia (95%O2/5%CO2) or normoxia (21%O2) in vitro. Cells and culture media were recovered separately for assays of ACE-2, TNF-α-converting enzyme (TACE), αSmooth muscle actin (αSMA)-myofibroblast marker-, N-cadherin, and β-catenin immunoreactive protein.
resultsACE-2 significantly increased when IMR-90 were hypoxic prior to hyperoxic exposure with no recovery. In contrast to hyperoxia alone, ACE-2 did not decrease when IMR-90 were hypoxic prior to hyperoxic exposure with recovery. TACE/ADAM17 protein and mRNA were significantly decreased under these conditions. αSMA N-cadherin, and β-catenin proteins were significantly decreased with or without normoxic recovery.
conclusionsHypoxia prior to hyperoxic exposure of fetal lung fibroblasts prevented ACE-2 downregulation and decreased ADAM17/TACE protein and mRNA. αSMA, N-cadherin, and β-catenin were also significantly decreased under these conditions.
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