Kbg and Kv1.3 channels mediate potassium efflux in the early phase of apoptosis in Jurkat T lymphocytes

被引:38
|
作者
Valencia-Cruz, Georgina [1 ]
Shabala, Lana [2 ]
Delgado-Enciso, Ivan [3 ]
Shabala, Sergey [2 ]
Bonales-Alatorre, Edgar [1 ]
Pottosin, Igor I. [1 ]
Dobrovinskaya, Oxana R. [1 ]
机构
[1] Univ Colima, Ctr Biomed Res, Colima 28045, Mexico
[2] Univ Tasmania, Sch Agr Sci, Hobart, Tas, Australia
[3] Univ Colima, Sch Med, Colima 28045, Mexico
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 2009年 / 297卷 / 06期
关键词
staurosporine; Jurkat cells; K+ background current; STAUROSPORINE-INDUCED APOPTOSIS; ION-SELECTIVE MICROELECTRODES; CELLULAR TAURINE RELEASE; CASPASE ACTIVATION; VOLUME REGULATION; DEATH RECEPTORS; U937; CELLS; IN-VITRO; FLUXES; STIMULATION;
D O I
10.1152/ajpcell.00064.2009
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Valencia-Cruz G, Shabala L, Delgado-Enciso I, Shabala S, Bonales-Alatorre E, Pottosin II, Dobrovinskaya OR. K-bg and Kv1.3 channels mediate potassium efflux in the early phase of apoptosis in Jurkat T lymphocytes. Am J Physiol Cell Physiol 297: C1544-C1553, 2009. First published September 30, 2009; doi:10.1152/ajpcell.00064.2009.-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 mu M) 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 (K-bg) 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 K-bg and Kv1.3 channels to the transient and posttransient STS-induced K+ efflux components, respectively, was confirmed by the effects of bupivacaine, predominantly blocking K-bg current, and the Kv1.3-specific blocker margatoxin. Channel-mediated K+ efflux provoked a substantial cellular shrinkage and affected the activation of caspases.
引用
收藏
页码:C1544 / C1553
页数:10
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