ArticleAmerican journal of respiratory cell and molecular biology2012
Regulation of alveolar epithelial Na+ channels by ERK1/2 in chlorine-breathing mice.
Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 47 citations in OpenAlex.
- Connexin-hemichannels-mediated ATP release causes lung injury following chlorine inhalation.American journal of physiology. Cell physiology · 2025Article
- The long road to Ithaca: a physiologist's journey.American journal of physiology. Cell physiology · 2025Review
- Toward in vivo bronchoscopic functional CFTR assessment using a short circuit current measurement probe.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Carbon dioxide and MAPK signalling: towards therapy for inflammation.Cell communication and signaling : CCS · 2023Review
- Submersion and hypoxia inhibit alveolar epithelial NaRespiratory research · 2023Article
- AICAR decreases acute lung injury by phosphorylating AMPK and upregulating heme oxygenase-1.The European respiratory journal · 2021Article
- Halogen-Induced Chemical Injury to the Mammalian Cardiopulmonary Systems.Physiology (Bethesda, Md.) · 2021Review
- Article
- Hyaluronan and halogen-induced airway hyperresponsiveness and lung injury.Annals of the New York Academy of Sciences · 2020Review
- Chemical warfare agent research in precision-cut tissue slices-a useful alternative approach.Annals of the New York Academy of Sciences · 2020Review
- Vascular permeability disruption explored in the proteomes of mouse lungs and human microvascular cells following acute bromine exposure.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Phosgene inhalation causes hemolysis and acute lung injury.Toxicology letters · 2019Article
- Article
- Influenza-mediated reduction of lung epithelial ion channel activity leads to dysregulated pulmonary fluid homeostasis.JCI insight · 2018Article
- Influenza virus infection alters ion channel function of airway and alveolar cells: mechanisms and physiological sequelae.American journal of physiology. Lung cellular and molecular physiology · 2017Review
- Alveolar nonselective channels are ASIC1a/α-ENaC channels and contribute to AFC.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Formaldehyde impairs transepithelial sodium transport.Scientific reports · 2016Article
- Chlorine-induced cardiopulmonary injury.Annals of the New York Academy of Sciences · 2016Review
- Role of epithelial sodium channels in the regulation of lung fluid homeostasis.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Upregulation of autophagy decreases chlorine-induced mitochondrial injury and lung inflammation.Free radical biology & medicine · 2015Article
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
The mechanisms by which the exposure of mice to Cl(2) decreases vectorial Na(+) transport and fluid clearance across their distal lung spaces have not been elucidated. We examined the biophysical, biochemical, and physiological changes of rodent lung epithelial Na(+) channels (ENaCs) after exposure to Cl(2), and identified the mechanisms involved. We measured amiloride-sensitive short-circuit currents (I(amil)) across isolated alveolar Type II (ATII) cell monolayers and ENaC single-channel properties by patching ATII and ATI cells in situ. α-ENaC, γ-ENaC, total and phosphorylated extracellular signal-related kinase (ERK)1/2, and advanced products of lipid peroxidation in ATII cells were measured by Western blot analysis. Concentrations of reactive intermediates were assessed by electron spin resonance (ESR). Amiloride-sensitive Na(+) channels with conductances of 4.5 and 18 pS were evident in ATI and ATII cells in situ of air-breathing mice. At 1 hour and 24 hours after exposure to Cl(2), the open probabilities of these two channels decreased. This effect was prevented by incubating lung slices with inhibitors of ERK1/2 or of proteasomes and lysosomes. The exposure of ATII cell monolayers to Cl(2) increased concentrations of reactive intermediates, leading to ERK1/2 phosphorylation and decreased I(amil) and α-ENaC concentrations at 1 hour and 24 hours after exposure. The administration of antioxidants to ATII cells before and after exposure to Cl(2) decreased concentrations of reactive intermediates and ERK1/2 activation, which mitigated the decrease in I(amil) and ENaC concentrations. The reactive intermediates formed during and after exposure to Cl(2) activated ERK1/2 in ATII cells in vitro and in vivo, leading to decreased ENaC concentrations and activity.
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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.