We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Effect of dexamethasone on voltage-gated K<sup>+</sup> channels in Jurkat T-lymphocytes.
- Authors
Lampert, Angelika; Müller, Matthias M.; Berchtold, Susanne; Lang, Karl S.; Palmada, Monica; Dobrovinskaya, Oxana; Lang, Florian
- Abstract
The voltage-gated K+ channel Kv1.3 is an important regulator of lymphocyte function. Activation of lymphocytes is accompanied by stimulation, whereas CD95-induced apoptosis by inhibition, of Kv1.3. The channel serves to maintain cell membrane potential, a prerequisite for signalling through the Ca2+ release-activated Ca2+ channel ICRAC. As glucocorticoids are known to regulate lymphocyte function, the present study addressed the effect of dexamethasone on voltage-gated K+ channels in Jurkat T-lymphocytes. In whole-cell patch-clamp experiments current families evoked by 200-ms potential steps every 15 s from -70 mV to values from -120 to +100 mV revealed the functional expression of voltage-gated K+ channels. Pre-treatment of Jurkat T-lymphocytes for 2–3 h with 1 µM dexamethasone led to a significant decrease of voltage-gated K+ currents. Fura-2-fluorescence measurements showed that the readdition of Ca2+ to Ca2+-depleted cells led to a rapid increase of cytosolic Ca2+ activity. This increase of Ca2+ activity was blunted by both the K+ channel blocker margatoxin (10 nM) and 24 h pre-treatment with dexamethasone (1 µM). In conclusion, dexamethasone inhibits voltage-gated K+ channels in Jurkat T-lymphocytes, an effect impeding Ca2+ entry through ICRAC.
- Publication
Pflügers Archiv: European Journal of Physiology, 2003, Vol 447, Issue 2, p168
- ISSN
0031-6768
- Publication type
Academic Journal
- DOI
10.1007/s00424-003-1148-2