Primary pathways of intracellular Ca(2+) mobilization by nanosecond pulsed electric field.
Primary pathways of intracellular Ca(2+) mobilization by nanosecond pulsed electric field.
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DOI：
10.1016/j.bbamem.2012.11.032
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发表时间：
2013-03
影响因子：
3.4
通讯作者：
Pakhomov, Andrei G.
中科院分区：
文献类型：
--
作者：
Semenov, Iurii;Xiao, Shu;Pakhomov, Andrei G.
Permeabilization of cell membranous structures by nanosecond pulsed electric field (nsPEF) triggers transient rise of cytosolic Ca2+ concentration ([Ca2+]i), which determines multifarious downstream effects. Using fast ratiometric Ca2+ imaging with Fura-2, we quantified the external Ca2+ uptake, compared it with Ca2+ release from the endoplasmic reticulum (ER), and analyzed the interplay of these processes. We utilized CHO cells which lack voltage-gated Ca2+ channels, so that nsPEF-induced [Ca2+]i changes could be attributed primarily to electroporation. We found that a single 60-ns pulse caused fast [Ca2+]i increase by Ca2+ influx from the outside and Ca2+ efflux from the ER, with the E-field thresholds of about 9 and 19 kV/cm, respectively. Above these thresholds, the amplitude of [Ca2+]i response increased linearly by 8–10 nM per 1 kV/cm until a critical level between 200 and 300 nM of [Ca2+]i was reached. If the critical level was reached, the nsPEF-induced Ca2+ signal was amplified up to 3,000 nM by engaging the physiological mechanism of Ca2+-induced Ca2+-release (CICR). The amplification was prevented by depleting Ca2+ from the ER store with 100 nM thapsigargin, as well as by blocking the ER inositol-1,4,5-trisphosphate receptors (IP3R) with 50 μM of 2-aminoethoxydiphenyl borate (2-APB). Mobilization of [Ca2+]i by nsPEF mimicked native Ca2+ signaling, but without preceding activation of plasma membrane receptors or channels. NsPEF stimulation may serve as a unique method to activate [Ca2+]i and downstream cascades while bypassing the plasma membrane receptors.
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影响因子：
5
作者：
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通讯作者：
Pakhomov, Andrei G.
影响因子：
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DOI：
10.1016/j.vascn.2004.08.008
发表时间：
2005-05-05
影响因子：
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作者：
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通讯作者：
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