TY - JOUR
T1 - Kbg and Kv1.3 channels mediate potassium efflux in the early phase of apoptosis in Jurkat T lymphocytes
AU - Valencia-Cruz, Georgina
AU - Shabala, Lana
AU - Delgado-Enciso, Ivan
AU - Shabala, Sergey
AU - Bonales-Alatorre, Edgar
AU - Pottosin, Igor I.
AU - Dobrovinskaya, Oxana R.
PY - 2009
Y1 - 2009
N2 - Microelectrode ion flux estimation (MIFE) and patch-clamp techniques were combined for noninvasive K+ flux measurements and recording of activities of the dominant K+ channels in the early phases of apoptosis in Jurkat cells. Staurosporine (STS, 1 μM) evoked rapid (peaking around 15 min) transient K+ efflux, which then gradually decreased. This transient K+ efflux occurred concurrently with the transient increase of the K+ background (Kbg) TWIK-related spinal cord K + channel-like current density, followed by a drastic decrease and concomitant membrane depolarization. The Kv1.3 current density remained almost constant. Kv1.3 activation was not altered by STS, whereas the inactivation was shifted to more positive potentials. Contribution of Kbg and Kv1.3 channels to the transient and posttransient STS-induced K+ efflux components, respectively, was confirmed by the effects of bupivacaine, predominantly blocking Kbg current, and the Kv1.3-specific blocker margatoxin. Channel-mediated K+ efflux provoked a substantial cellular shrinkage and affected the activation of caspases.
AB - Microelectrode ion flux estimation (MIFE) and patch-clamp techniques were combined for noninvasive K+ flux measurements and recording of activities of the dominant K+ channels in the early phases of apoptosis in Jurkat cells. Staurosporine (STS, 1 μM) evoked rapid (peaking around 15 min) transient K+ efflux, which then gradually decreased. This transient K+ efflux occurred concurrently with the transient increase of the K+ background (Kbg) TWIK-related spinal cord K + channel-like current density, followed by a drastic decrease and concomitant membrane depolarization. The Kv1.3 current density remained almost constant. Kv1.3 activation was not altered by STS, whereas the inactivation was shifted to more positive potentials. Contribution of Kbg and Kv1.3 channels to the transient and posttransient STS-induced K+ efflux components, respectively, was confirmed by the effects of bupivacaine, predominantly blocking Kbg current, and the Kv1.3-specific blocker margatoxin. Channel-mediated K+ efflux provoked a substantial cellular shrinkage and affected the activation of caspases.
KW - Jurkat cells
KW - K background current
KW - Staurosporine
UR - http://www.scopus.com/inward/record.url?scp=73449099670&partnerID=8YFLogxK
U2 - 10.1152/ajpcell.00064.2009
DO - 10.1152/ajpcell.00064.2009
M3 - Article
C2 - 19794143
AN - SCOPUS:73449099670
SN - 0363-6143
VL - 297
SP - C1544-C1553
JO - American Journal of Physiology - Cell Physiology
JF - American Journal of Physiology - Cell Physiology
IS - 6
ER -