ArticleActa physiologica (Oxford, England)2016
The calcium-activated potassium channel KCa3.1 plays a central role in the chemotactic response of mammalian neutrophils.
Article in Acta physiologica (Oxford, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- KArchiv der Pharmazie · 2026Article
- A new perspective on mesenchymal stem cells and their derivatives in alleviating cerebral ischemia-reperfusion injury dynamically regulating mitochondrial function to remodel the immune network.Cell death & disease · 2026Review
- Inwardly rectifying potassium channels promote directional sensing during neutrophil chemotaxis.The Journal of cell biology · 2026Article
- Inwardly rectifying potassium channels regulate membrane potential polarization and direction sensing during neutrophil chemotaxis.bioRxiv : the preprint server for biology · 2025Article
- Membrane potential dynamics of C5a-stimulated neutrophil granulocytes.Pflugers Archiv : European journal of physiology · 2024Article
- Efficacy of combined tumor irradiation and KScientific reports · 2023Article
- The voltage-gated potassium channel KV1.3 regulates neutrophil recruitment during inflammation.Cardiovascular research · 2022Article
- Regulatory role of KCa3.1 in immune cell function and its emerging association with rheumatoid arthritis.Frontiers in immunology · 2022Review
- Treatment with senicapoc in a porcine model of acute respiratory distress syndrome.Intensive care medicine experimental · 2021Article
- Article
- Ion Channels Orchestrate Pancreatic Ductal Adenocarcinoma Progression and Therapy.Frontiers in pharmacology · 2020Review
- Cancer-Associated Intermediate Conductance CaCancers · 2019Review
- Calcium signalling and related ion channels in neutrophil recruitment and function.European journal of clinical investigation · 2018Review
- Kcnn4 is a modifier gene of intestinal cystic fibrosis preventing lethality in the Cftr-F508del mouse.Scientific reports · 2018Article
- Structure, Gating and Basic Functions of the Ca2+-activated K Channel of Intermediate Conductance.Current neuropharmacology · 2018Review
- Tamoxifen inhibits chemokinesis in equine neutrophils.Irish veterinary journal · 2018Article
- Pro-inflammatory CaScientific reports · 2017Article
- Functional Cooperation between KCa3.1 and TRPV4 Channels in Bronchial Smooth Muscle Cell Proliferation Associated with Chronic Asthma.Frontiers in pharmacology · 2017Article
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9 authors at 3 institutions in 2 countries.
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Abstract
aimNeutrophils are the first cells to arrive at sites of injury. Nevertheless, many inflammatory diseases are characterized by an uncontrolled infiltration and action of these cells. Cell migration depends on volume changes that are governed by ion channel activity, but potassium channels in neutrophil have not been clearly identified. We aim to test whether KCa3.1 participates in neutrophil migration and other relevant functions of the cell.
methodsCytometer and confocal measurements to determine changes in cell volume were used. Cells isolated from human, mouse and horse were tested for KCa3.1-dependent chemotaxis. Chemokinetics, calcium handling and release of reactive oxygen species were measured to determine the role of KCa3.1 in those processes. A mouse model was used to test for neutrophil recruitment after acute lung injury in vivo.
resultsWe show for the first time that KCa3.1 is expressed in mammalian neutrophils. When the channel is inhibited by a pharmacological blocker or by genetic silencing, it profoundly affects cell volume regulation, and chemotactic and chemokinetic properties of the cells. We also demonstrated that pharmacological inhibition of KCa3.1 did not affect calcium entry or reactive oxygen species production in neutrophils. Using a mouse model of acute lung injury, we observed that Kca3.1(-/-) mice are significantly less effective at recruiting neutrophils into the site of inflammation.
conclusionsThese results demonstrate that KCa3.1 channels are key actors in the migration capacity of neutrophils, and its inhibition did not affect other relevant cellular functions.
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