Authors
Tahir Ulu, Henrik Siemer, Alexa Heuer, Sandra Schimmelpfennig, Peter Dieterich, Jesús Borrego, György Panyi, Albrecht Schwab
Published in
Archiv der Pharmazie. Volume 359. Issue 10. Pages e70365.
Abstract
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.
PMID:
42885434
Bibliographic data and abstract were imported from PubMed on 16 Oct 2026.
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