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K+ Channels in Membrane Potential Dynamics and Migration of Neutrophil Granulocytes.

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Τίτλος: K+ Channels in Membrane Potential Dynamics and Migration of Neutrophil Granulocytes.
Συγγραφείς: Ulu T; Institut für Physiologie II, University Münster, Münster, Germany., Siemer H; Institut für Physiologie II, University Münster, Münster, Germany., Heuer A; Institut für Physiologie II, University Münster, Münster, Germany., Schimmelpfennig S; Institut für Physiologie II, University Münster, Münster, Germany., Dieterich P; Institut für Physiologie, TU Dresden, Dresden, Germany., Borrego J; Department of Biophysics and Cell Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary., Panyi G; Department of Biophysics and Cell Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary., Schwab A; Institut für Physiologie II, University Münster, Münster, Germany.
Πηγή: Archiv der Pharmazie [Arch Pharm (Weinheim)] 2026 Oct; Vol. 359 (10), pp. e70365.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Wiley-VCH Verlag GmbH & Co. KGaA Country of Publication: Germany NLM ID: 0330167 Publication Model: Print Cited Medium: Internet ISSN: 1521-4184 (Electronic) Linking ISSN: 03656233 NLM ISO Abbreviation: Arch Pharm (Weinheim) Subsets: MEDLINE
Imprint Name(s): Publication: <2005->: Weinheim Germany : Wiley-VCH Verlag GmbH & Co. KGaA
Original Publication: Weinheim, Verlag Chemie GmbH.
Ιατρικοί όροι (MeSH): Neutrophils*/metabolism , Neutrophils*/drug effects , Neutrophils*/physiology , Membrane Potentials*/drug effects , Potassium Channels, Inwardly Rectifying*/metabolism , Potassium Channels, Inwardly Rectifying*/antagonists & inhibitors , Intermediate-Conductance Calcium-Activated Potassium Channels*/metabolism , Intermediate-Conductance Calcium-Activated Potassium Channels*/antagonists & inhibitors , Kv1.3 Potassium Channel*/metabolism , Kv1.3 Potassium Channel*/antagonists & inhibitors, Leukotriene B4/metabolism ; Complement C5a/metabolism ; Complement C5a/pharmacology ; Potassium Channel Blockers/pharmacology ; Humans ; Chemotaxis ; Cell Movement
Περίληψη: Neutrophil granulocytes exhibit dynamic changes in membrane potential upon stimulation with the complement component C5a. It is not well-defined which ion channels are responsible for membrane potential dynamics in neutrophils, although ion channel signaling has been linked to neutrophil behavior. Here, we investigated the contribution of K+ channels that are important players in different immune cells: KCa3.1, Kir2.1, and KV1.3. We studied their roles in membrane potential regulation, chemotaxis, and LTB4 secretion using live-cell imaging, analytical methods, and mathematical modeling. We identify membrane potential dynamics as an important regulatory axis in neutrophil migration. Kir2.1 is a key regulator of resting membrane potential. Kir2.1 blockade depolarizes the membrane potential of neutrophils by ~30 mV to -41.9 mV, and it delays and attenuates the C5a-induced depolarization. In contrast, KCa3.1 and KV1.3 inhibition neither modifies the resting membrane potential nor the C5a-induced depolarization. Nonetheless, the inhibition of all three K+ channels impairs chemotaxis toward C5a, in part by a reduced LTB4 secretion and/or possibly by non-conductive properties related to the interactome of the three K+ channels. Together, these findings demonstrate that KCa3.1, KV1.3 and Kir2.1 channels play distinct but critical roles in neutrophil function and inflammatory signalling.
(© 2026 The Author(s). Archiv der Pharmazie published by Wiley‐VCH GmbH on behalf of Deutsche Pharmazeutische Gesellschaft.)
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Grant Information: GRK 2515/2 Deutsche Forschungsgemeinschaft; Chembion Deutsche Forschungsgemeinschaft; 2024-1.2.3-HU-RIZONT-2024-00099 Ministry of Culture and Innovation of Hungary; MedK, Medical Faculty of the University of Münster
Contributed Indexing: Keywords: KCa3.1; Kir2.1; Kv1.3; LTB4; Neutrophil granulocyte; chemotaxis; membrane potential dynamics
Substance Nomenclature: 1HGW4DR56D (Leukotriene B4)
0 (Potassium Channels, Inwardly Rectifying)
80295-54-1 (Complement C5a)
0 (Intermediate-Conductance Calcium-Activated Potassium Channels)
0 (Kir2.1 channel)
0 (Kv1.3 Potassium Channel)
0 (Potassium Channel Blockers)
0 (KCNN4 protein, human)
Entry Date(s): Date Created: 20261016 Date Completed: 20261016 Latest Revision: 20261019
Update Code: 20261019
PubMed Central ID: PMC13673283
DOI: 10.1002/ardp.70365
PMID: 42885434
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:1521-4184
DOI:10.1002/ardp.70365