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Immunomodulation of voltage-dependent K+ channels in macrophages: molecular and biophysical consequences

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dc.contributor.author Villalonga, Núria
dc.contributor.author David, Miren
dc.contributor.author Bielanska, Joanna
dc.contributor.author Vicente García, Rubén, 1978-
dc.contributor.author Comes, Núria
dc.contributor.author Valenzuela, Carmen
dc.contributor.author Felipe, Antonio
dc.date.accessioned 2016-01-18T15:25:16Z
dc.date.available 2016-01-18T15:25:16Z
dc.date.issued 2010
dc.identifier.citation Villalonga N, David M, Bielanska J, Vicente R, Comes N, Valenzuela C et al. Immunomodulation of voltage-dependent K+ channels in macrophages: molecular and biophysical consequences. Journal of general physiology. 2010;135(2):135-47. DOI: 10.1085/jgp.200910334
dc.identifier.issn 0022-1295
dc.identifier.uri http://hdl.handle.net/10230/25593
dc.description.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.
dc.description.sponsorship This work was supported by the Ministerio de Ciencia e Innovación (MICINN), Spain (grants BFU2005-00695, BFU2008-00431, and CSD2008-00005 to A. Felipe, and grants SAF2007-65868 and FIS D06/0014/0006 to C. Valenzuela). N. Villalonga and J. Bielanska held fellowships from the MICINN. M. David held an FIS RD06/0014/0006 contract. N. Comes is supported by the Juan de la Cierva program (MICINN)
dc.format.mimetype application/pdf
dc.language.iso eng
dc.publisher Rockefeller University Press
dc.relation.ispartof Journal of general physiology. 2010;135(2):135-47
dc.rights © Villalonga et al., 2010. This article is distributed under a Creative Commons License Attribution–Noncommercial–Share Alike 3.0 Unported.
dc.rights.uri http://creativecommons.org/licenses/by-nc-sa/3.0/
dc.subject.other Canals de potassi
dc.title Immunomodulation of voltage-dependent K+ channels in macrophages: molecular and biophysical consequences
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.1085/jgp.200910334
dc.relation.projectID info:eu-repo/grantAgreement/ES/2PN/BFU2005-00695
dc.relation.projectID info:eu-repo/grantAgreement/ES/2PN/SAF2007-65868
dc.relation.projectID info:eu-repo/grantAgreement/ES/3PN/BFU2008-00431
dc.relation.projectID info:eu-repo/grantAgreement/ES/3PN/CSD2008-00005
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/publishedVersion


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