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Developmental Switch of the Expression of Ion Channels in Human Dendritic Cells¹

Emese Zsiros^2,*, Katalin Kis-Toth^2,, Peter Hajdu^*, Rezso Gaspar^*, Joanna Bielanska, Antonio Felipe, Eva Rajnavolgyi and Gyorgy Panyi^3,*,

^* Department of Biophysics and Cell Biology, University of Debrecen, Debrecen, Hungary; Department of Immunology, University of Debrecen, Debrecen, Hungary; Molecular Physiology Laboratory, Department of Biochemistry and Molecular Biology, Institute of Biomedicine, University of Barcelona, Barcelona, Spain; and Cell Biology and Signaling Research Group of the Hungarian Academy of Sciences, Research Center for Molecular Medicine, University of Debrecen, Debrecen, Hungary

Modulation of the expression and activity of plasma membrane ion channels is one of the mechanisms by which immune cells can regulate their intracellular Ca²⁺ signaling pathways required for proliferation and/or differentiation. Voltage-gated K⁺ channels, inwardly rectifying K⁺ channels, and Ca²⁺-activated K⁺ channels have been described to play a major role in controlling the membrane potential in lymphocytes and professional APCs, such as monocytes, macrophages, and dendritic cells (DCs). Our study aimed at the characterization and identification of ion channels expressed in the course of human DC differentiation from monocytes. We report in this study for the first time that immature monocyte-derived DCs express voltage-gated Na⁺ channels in their plasma membrane. The analysis of the biophysical and pharmacological properties of the current and PCR-based cloning revealed the presence of Nav1.7 channels in immature DCs. Transition from the immature to a mature differentiation state, however, was accompanied by the down-regulation of Nav1.7 expression concomitant with the up-regulation of voltage-gated Kv1.3 K⁺ channel expression. The presence of Kv1.3 channels seems to be common for immune cells; hence, selective Kv1.3 blockers may emerge as candidates for inhibiting various functions of mature DCs that involve their migratory, cytokine-secreting, and T cell-activating potential.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by the following grants: OTKA K 60740, NK 61412, and Társadalmi Megújulás Operatív Program-4.2.2-08/1/2008-0019 (to G.P.), ETT/064/2006 (to R.G.), NKFP 00427/2004 and OTKA NK72937 (to E.R.), and BFU2008-00431 and CSD2008-00005 from Ministerio de Ciencia e Innovación (Spain; to A.F.).

² E.Z. and K.K.-T. contributed equally to this manuscript.

³ Address correspondence and reprint requests to Dr. Gyorgy Panyi, University of Debrecen, Medical and Health Science Center, Department of Biophysics and Cell Biology, 98. Nagyerdei krt., Debrecen, 4012, Hungary. E-mail address: panyi{at}med.unideb.hu

⁴ Abbreviations used in this paper: DC, dendritic cell; ChTx, charybdotoxin; Ct, cycle threshold; EC, extracellular; IDC, immature DC; IPI, interpulse interval; MDC, mature DC; MgTx, margatoxin; RCF, remaining current fraction; RF, recovered fraction; TEA, tetraethylammonium; TTX, tetrodotoxin; VGPC, voltage-gated K⁺ channel; VGSC, voltage-gated sodium channel.