ArticleCardiovascular research2022
The voltage-gated potassium channel KV1.3 regulates neutrophil recruitment during inflammation.
Article in Cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- KArchiv der Pharmazie · 2026Article
- Potassium channels in cancer: from hallmarks to therapeutic targeting.Journal of physiology and biochemistry · 2026Review
- Article
- Kv1.3 regulates macrophage immune function through PI3K/AKT signaling pathway to alleviate metabolic dysfunction-associated steatohepatitis.Journal of molecular medicine (Berlin, Germany) · 2026Article
- The dual non-competitive CXCR1/2 inhibitor ladarixin impairs neutrophil extravasation without altering intravascular adhesion.Haematologica · 2026Article
- Inwardly rectifying potassium channels promote directional sensing during neutrophil chemotaxis.The Journal of cell biology · 2026Article
- Mechanistic correlation of potassium channel sensing and nitric oxide activity in neuroinflammation.Molecular biology reports · 2025Review
- Specific macrophage RhoA targeting CRISPR-Cas9 for mitigating osteoclastogenesis-induced joint damage in inflammatory arthritis.Cell reports. Medicine · 2025Article
- Inwardly rectifying potassium channels regulate membrane potential polarization and direction sensing during neutrophil chemotaxis.bioRxiv : the preprint server for biology · 2025Article
- ShK-modified UCMSCs Inhibit M1-Like Macrophage Polarization and Alleviate Osteoarthritis Progression via PI3K/Akt Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Nanoscopy reveals integrin clustering reliant on kindlin-3 but not talin-1.Cell communication and signaling : CCS · 2025Article
- Omega 3 fatty acid docosahexaenoic acid (DHA) mitigates inflammatory responses in experimental sepsis.Frontiers in pharmacology · 2025Article
- Cytosolic S100A8/A9 promotes CaeLife · 2024Article
- The eATP/P2×7R Axis Drives Quantum Dot-Nanoparticle Induced Neutrophil Recruitment in the Pulmonary Microcirculation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Neutrophils-biology and diversity.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024Review
- Review
- Membrane potential dynamics of C5a-stimulated neutrophil granulocytes.Pflugers Archiv : European journal of physiology · 2024Article
- CCR3-dependent eosinophil recruitment is regulated by sialyltransferase ST3Gal-IV.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- An Ultrasensitive Genetically Encoded Voltage Indicator Uncovers the Electrical Activity of Non-Excitable Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The role of potassium ion channels in chronic sinusitis.Frontiers in pharmacology · 2024Review
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Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
Abstract
aimsNeutrophil trafficking within the vasculature strongly relies on intracellular calcium signalling. Sustained Ca2+ influx into the cell requires a compensatory efflux of potassium to maintain membrane potential. Here, we aimed to investigate whether the voltage-gated potassium channel KV1.3 regulates neutrophil function during the acute inflammatory process by affecting sustained Ca2+ signalling. METHODS AND
resultsUsing in vitro assays and electrophysiological techniques, we show that KV1.3 is functionally expressed in human neutrophils regulating sustained store-operated Ca2+ entry through membrane potential stabilizing K+ efflux. Inhibition of KV1.3 on neutrophils by the specific inhibitor 5-(4-Phenoxybutoxy)psoralen (PAP-1) impaired intracellular Ca2+ signalling, thereby preventing cellular spreading, adhesion strengthening, and appropriate crawling under flow conditions in vitro. Using intravital microscopy, we show that pharmacological blockade or genetic deletion of KV1.3 in mice decreased neutrophil adhesion in a blood flow dependent fashion in inflamed cremaster muscle venules. Furthermore, we identified KV1.3 as a critical component for neutrophil extravasation into the inflamed peritoneal cavity. Finally, we also revealed impaired phagocytosis of Escherichia coli particles by neutrophils in the absence of KV1.3.
conclusionWe show that the voltage-gated potassium channel KV1.3 is critical for Ca2+ signalling and neutrophil trafficking during acute inflammatory processes. Our findings do not only provide evidence for a role of KV1.3 for sustained calcium signalling in neutrophils affecting key functions of these cells, they also open up new therapeutic approaches to treat inflammatory disorders characterized by overwhelming neutrophil infiltration.
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