Differential Activity of Voltage- and Ca2+-Dependent Potassium Channels in Leukemic T Cell Lines: Jurkat Cells Represent an Exceptional Case

• Published in: Frontiers in physiology Vol. 9; p. 499
• Main Authors: Valle-Reyes, Salvador, Valencia-Cruz, Georgina, Liñan-Rico, Liliana, Pottosin, Igor, Dobrovinskaya, Oxana
• Format: Journal Article
• Language: English
• Published: Frontiers Media S.A 09.05.2018
• Subjects: calcium signaling; current density; Physiology; potassium channel; T leukemia; T lymphocyte; voltage gating
• ISSN: 1664-042X; 1664-042X
• DOI: 10.3389/fphys.2018.00499

Activation of resting T cells relies on sustained Ca 2+ influx across the plasma membrane, which in turn depends on the functional expression of potassium channels, whose activity repolarizes the membrane potential. Depending on the T-cells subset, upon activation the expression of Ca 2+ - or voltage-activated K + channels, KCa or Kv, is up-regulated. In this study, by means of patch-clamp technique in the whole cell mode, we have studied in detail the characteristics of Kv and KCa currents in resting and activated human T cells, the only well explored human T-leukemic cell line Jurkat, and two additional human leukemic T cell lines, CEM and MOLT-3. Voltage dependence of activation and inactivation of Kv1.3 current were shifted up to by 15 mV to more negative potentials upon a prolonged incubation in the whole cell mode and displayed little difference at a stable state in all cell lines but CEM, where the activation curve was biphasic, with a high and low potential components. In Jurkat, KCa currents were dominated by apamine-sensitive KCa2.2 channels, whereas only KCa3.1 current was detected in healthy T and leukemic CEM and MOLT-3 cells. Despite a high proliferation potential of Jurkat cells, Kv and KCa currents were unexpectedly small, more than 10-fold lesser as compared to activated healthy human T cells, CEM and MOLT-3, which displayed characteristic Kv1.3 high :KCa3.1 high phenotype. Our results suggest that Jurkat cells represent perhaps a singular case and call for more extensive studies on primary leukemic T cell lines as well as a verification of the therapeutic potential of specific KCa3.1 blockers to combat acute lymphoblastic T leukemias.