ArticleAmerican journal of translational research2013
Regulation of Monocyte Chemotactic Protein-1 secretion by the Two-Pore-Domain Potassium (K2P) channel TREK-1 in human alveolar epithelial cells.
Article in American journal of translational research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 23 citations in OpenAlex.
- 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
- 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 Endothelial Large Conductance Potassium Channels Protects against TNF-α-Induced Inflammation.International journal of molecular sciences · 2023Article
- 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
- Negative Influence by the Force: Mechanically Induced Hyperpolarization via KInternational journal of molecular sciences · 2021Review
- 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
- TREK1 channel activation as a new analgesic strategy devoid of opioid adverse effects.British journal of pharmacology · 2020Article
- Mechanism of Cxc Chemokine Ligand 5 (CXCL5)/Cxc Chemokine Receptor 2 (CXCR2) Bio-Axis in Mice with Acute Respiratory Distress Syndrome.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- 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
- Pathophysiology and Management of Acute Respiratory Distress Syndrome in Children.Pediatric clinics of North America · 2017Review
- 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
- Pulmonary epithelial barrier function: some new players and mechanisms.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Interactions of Francisella tularensis with Alveolar Type II Epithelial Cells and the Murine Respiratory Epithelium.PloS one · 2015Article
- TREK-1 Regulates Cytokine Secretion from Cultured Human Alveolar Epithelial Cells Independently of Cytoskeletal Rearrangements.PloS one · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We recently proposed a role for the 2-pore-domain K(+) (K2P) channel TREK-1 in the regulation of cytokine release from alveolar epithelial cells (AECs) by demonstrating decreased IL-6 secretion from TREK-1 deficient cells, but the effects of altered TREK-1 expression on other inflammatory mediators remain poorly understood. We now examined the role of TREK-1 in TNF-α-induced MCP-1 release from human A549 cells. We hypothesized that TREK-1 regulates TNF-α-induced MCP-1 secretion via c-Jun N-terminal kinases (JNK)- and protein kinase-C (PKC)-dependent pathways. In contrast to IL-6 secretion, we found that TREK-1 deficiency resulted in increased MCP-1 production and secretion, although baseline MCP-1 gene expression was unchanged in TREK-1 deficient cells. In contrast to TREK-1 deficient AECs, overexpression of MCP-1 had no effect on MCP-1 secretion. Phosphorylation of JNK1/2/3 was increased in TREK-1 deficient cells upon TNF-α stimulation, but pharmacological inhibition of JNK1/2/3 decreased MCP-1 release from both control and TREK-1 deficient cells. Similarly, pharmacological inhibition of PKC decreased MCP-1 secretion from control and TREK-1 deficient cells, suggesting that alterations in JNK and PKC signaling pathways were unlikely the cause for the increased MCP-1 secretion from TREK-1 deficient cells. Furthermore, MCP-1 secretion from control and TREK-1 deficient cells was independent of extracellular Ca(2+) but sensitive to inhibition of intracellular Ca(2+) reuptake mechanisms. In summary, we report for the first time that TREK-1 deficiency in human AECs resulted in increased MCP-1 production and secretion, and this effect appeared unrelated to alterations in JNK-, PKC- or Ca(2+)-mediated signaling pathways in TREK-1 deficient cells.
Indexed as
Identifiers
23977412PMC3745440W1820424831What OpenQuestion holds
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.