ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
Regulation and function of the two-pore-domain (K2P) potassium channel Trek-1 in alveolar epithelial cells.
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Emerging roles of mechanosensitive ion channels in ventilator induced lung injury: a systematic review.Frontiers in immunology · 2024Pooled it
- Trial
- KPharmaceuticals (Basel, Switzerland) · 2026Review
- Role of the two-pore domain potassium channel TREK-1 in hyperoxia- and mechanical stretch-induced alveolar epithelial injury.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Pharmacological activation of BK channels protects against LPS-induced pneumonia.Scientific reports · 2025Article
- Mechanisms of impaired alveolar fluid clearance.Anatomical record (Hoboken, N.J. : 2007) · 2025Review
- Two-pore potassium channel TREK-1 (K2P2.1) regulates NLRP3 inflammasome activity in macrophages.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Function of KvLQT1 potassium channels in a mouse model of bleomycin-induced acute lung injury.Frontiers in physiology · 2024Article
- Activation of TREK-1 (American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Emerging roles of mechanosensitive ion channels in acute lung injury/acute respiratory distress syndrome.Respiratory research · 2022Review
- BK Channels Regulate LPS-induced CCL-2 Release from Human Pulmonary Endothelial Cells.American journal of respiratory cell and molecular biology · 2021Article
- KScientific reports · 2020Article
- P2Y receptor regulation of K2P channels that facilitate KAmerican journal of physiology. Cell physiology · 2018Article
- Hyperoxia treatment of TREK-1/TREK-2/TRAAK-deficient mice is associated with a reduction in surfactant proteins.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- The role of stretch-activated ion channels in acute respiratory distress syndrome: finally a new target?American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Fluoxetine Protection in Decompression Sickness in Mice is Enhanced by Blocking TREK-1 Potassium Channel with the "spadin" Antidepressant.Frontiers in physiology · 2016Article
- Complementary roles of KCa3.1 channels and β1-integrin during alveolar epithelial repair.Respiratory research · 2015Article
- Role of K₂p channels in stimulus-secretion coupling.Pflugers Archiv : European journal of physiology · 2015Review
- Much more than a leak: structure and function of K₂p-channels.Pflugers Archiv : European journal of physiology · 2015Review
- Pulmonary epithelial barrier function: some new players and mechanisms.American journal of physiology. Lung cellular and molecular physiology · 2015Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Hyperoxia can lead to a myriad of deleterious effects in the lung including epithelial damage and diffuse inflammation. The specific mechanisms by which hyperoxia promotes these pathological changes are not completely understood. Activation of ion channels has been proposed as one of the mechanisms required for cell activation and mediator secretion. The two-pore-domain K(+) channel (K2P) Trek-1 has recently been described in lung epithelial cells, but its function remains elusive. In this study we hypothesized that hyperoxia affects expression of Trek-1 in alveolar epithelial cells and that Trek-1 is involved in regulation of cell proliferation and cytokine secretion. We found gene expression of several K2P channels in mouse alveolar epithelial cells (MLE-12), and expression of Trek-1 was significantly downregulated in cultured cells and lungs of mice exposed to hyperoxia. Similarly, proliferation cell nuclear antigen (PCNA) and Cyclin D1 expression were downregulated by exposure to hyperoxia. We developed an MLE-12 cell line deficient in Trek-1 expression using shRNA and found that Trek-1 deficiency resulted in increased cell proliferation and upregulation of PCNA but not Cyclin D1. Furthermore, IL-6 and regulated on activation normal T-expressed and presumably secreted (RANTES) secretion was decreased in Trek-1-deficient cells, whereas release of monocyte chemoattractant protein-1 was increased. Release of KC/IL-8 was not affected by Trek-1 deficiency. Overall, deficiency of Trek-1 had a more pronounced effect on mediator secretion than exposure to hyperoxia. This is the first report suggesting that the K(+) channel Trek-1 could be involved in regulation of alveolar epithelial cell proliferation and cytokine secretion, but a direct association with hyperoxia-induced changes in Trek-1 levels remains elusive.
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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.