ArticleThe Journal of general physiology2010
Immunomodulation of voltage-dependent K+ channels in macrophages: molecular and biophysical consequences.
Article in The Journal of general physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 84 citations in OpenAlex.
- The Immune System as a Proarrhythmic Mediator: A Novel Paradigm for the Development of New Antiarrhythmic Therapy.The Canadian journal of cardiology · 2026Review
- Cardiac resident macrophages: the emerging role in arrhythmogenesis.Frontiers in immunology · 2026Review
- Effect of Voltage-Gated KbioRxiv : the preprint server for biology · 2024Article
- 3,3',4,4'-tetrachlorobiphenyl (PCB77) enhances human Kv1.3 channel currents and alters cytokine production.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Article
- Acute Adenoviral Infection Elicits an Arrhythmogenic Substrate Prior to Myocarditis.Circulation research · 2024Article
- Nonmyocytes as electrophysiological contributors to cardiac excitation and conduction.American journal of physiology. Heart and circulatory physiology · 2023Review
- Novel insights into the electrophysiology of murine cardiac macrophages: relevance of voltage-gated potassium channels.Cardiovascular research · 2022Article
- The contribution of ion channels to shaping macrophage behaviour.Frontiers in pharmacology · 2022Review
- Electroimmunology and cardiac arrhythmia.Nature reviews. Cardiology · 2021Review
- KCNE4-dependent functional consequences of Kv1.3-related leukocyte physiology.Scientific reports · 2021Article
- The activation gate controls steady-state inactivation and recovery from inactivation in Shaker.The Journal of general physiology · 2020Article
- The Potassium Channel Kv1.5 Expression Alters During Experimental Autoimmune Encephalomyelitis.Neurochemical research · 2019Article
- Critical regulation of atherosclerosis by the KCa3.1 channel and the retargeting of this therapeutic target in in-stent neoatherosclerosis.Journal of molecular medicine (Berlin, Germany) · 2019Review
- Biochemical and physiological properties of KChemico-biological interactions · 2019Review
- Differential effect of Androctonus australis hector venom components on macrophage KEuropean biophysics journal : EBJ · 2019Article
- Caveolar targeting links Kv1.3 with the insulin-dependent adipocyte physiology.Cellular and molecular life sciences : CMLS · 2018Article
- Cardiolipotoxicity, Inflammation, and Arrhythmias: Role for Interleukin-6 Molecular Mechanisms.Frontiers in physiology · 2018Review
- A systems pharmacology-based approach to identify novel Kv1.3 channel-dependent mechanisms in microglial activation.Journal of neuroinflammation · 2017Article
- Ubiquitination mediates Kv1.3 endocytosis as a mechanism for protein kinase C-dependent modulation.Scientific reports · 2017Article
- Fludarabine Inhibits KFrontiers in pharmacology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-dependent potassium (K(v)) channels play a pivotal role in the modulation of macrophage physiology. Macrophages are professional antigen-presenting cells and produce inflammatory and immunoactive substances that modulate the immune response. Blockage of K(v) channels by specific antagonists decreases macrophage cytokine production and inhibits proliferation. Numerous pharmacological agents exert their effects on specific target cells by modifying the activity of their plasma membrane ion channels. Investigation of the mechanisms involved in the regulation of potassium ion conduction is, therefore, essential to the understanding of potassium channel functions in the immune response to infection and inflammation. Here, we demonstrate that the biophysical properties of voltage-dependent K(+) currents are modified upon activation or immunosuppression in macrophages. This regulation is in accordance with changes in the molecular characteristics of the heterotetrameric K(v)1.3/K(v)1.5 channels, which generate the main K(v) in macrophages. An increase in K(+) current amplitude in lipopolysaccharide-activated macrophages is characterized by a faster C-type inactivation, a greater percentage of cumulative inactivation, and a more effective margatoxin (MgTx) inhibition than control cells. These biophysical parameters are related to an increase in K(v)1.3 subunits in the K(v)1.3/K(v)1.5 hybrid channel. In contrast, dexamethasone decreased the C-type inactivation, the cumulative inactivation, and the sensitivity to MgTx concomitantly with a decrease in K(v)1.3 expression. Neither of these treatments apparently altered the expression of K(v)1.5. Our results demonstrate that the immunomodulation of macrophages triggers molecular and biophysical consequences in K(v)1.3/K(v)1.5 hybrid channels by altering the subunit stoichiometry.
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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.