Evidence map›Paper›PMID 23220180›Full record

ArticleBiochimica et biophysica acta2013

Primary pathways of intracellular Ca(2+) mobilization by nanosecond pulsed electric field.

Iurii Semenov, Shu Xiao, Andrei G Pakhomov

Abstract read
In one paragraph

Article in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

77 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Biophysical principles of pulsed field ablation.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026
    Review
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  4. Article
  5. Article
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  10. Article
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  12. Article
  13. Modulating CaBiophysical journal · 2024
    Article
  14. Article
  15. Real-time imaging of individual electropores proves their longevity in cells.Biochemical and biophysical research communications · 2024
    Article
  16. Article
  17. Article
  18. In Vitro Imaging and Molecular Characterization of CaInternational journal of molecular sciences · 2023
    Article
  19. Article
  20. Article

17 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Iurii SemenovFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA, USA. Iurii.semenov@gmail.com
Shu Xiao
Andrei G Pakhomov

Funding

Mechanisms and Implications of Nanoelectroporation in Living CellsR01GM088303 · NIGMS · OLD DOMINION UNIVERSITY · PI PAKHOMOV, ANDREI G · 2010 to 2013
$1.1M
Cell Death Induction by High-Voltage, Nanosecond-duration Electric PulsesR01CA125482 · NCI · OLD DOMINION UNIVERSITY · PI PAKHOMOV, ANDREI G · 2008 to 2011
$1.1M
NCI NIH HHS R01 CA125482NCI NIH HHS R01CA125482NIGMS NIH HHS R01 GM088303NIGMS NIH HHS R01GM088303
6 · The paper itself

Abstract

Permeabilization of cell membranous structures by nanosecond pulsed electric field (nsPEF) triggers transient rise of cytosolic Ca(2+) concentration ([Ca(2+)](i)), which determines multifarious downstream effects. By using fast ratiometric Ca(2+) imaging with Fura-2, we quantified the external Ca(2+) uptake, compared it with Ca(2+) release from the endoplasmic reticulum (ER), and analyzed the interplay of these processes. We utilized CHO cells which lack voltage-gated Ca(2+) channels, so that the nsPEF-induced [Ca(2+)](i) changes could be attributed primarily to electroporation. We found that a single 60-ns pulse caused fast [Ca(2+)](i) increase by Ca(2+) influx from the outside and Ca(2+) efflux from the ER, with the E-field thresholds of about 9 and 19kV/cm, respectively. Above these thresholds, the amplitude of [Ca(2+)](i) response increased linearly by 8-10nM per 1kV/cm until a critical level between 200 and 300nM of [Ca(2+)](i) was reached. If the critical level was reached, the nsPEF-induced Ca(2+) signal was amplified up to 3000nM by engaging the physiological mechanism of Ca(2+)-induced Ca(2+)-release (CICR). The amplification was prevented by depleting Ca(2+) from the ER store with 100nM thapsigargin, as well as by blocking the ER inositol-1,4,5-trisphosphate receptors (IP(3)R) with 50μM of 2-aminoethoxydiphenyl borate (2-APB). Mobilization of [Ca(2+)](i) by nsPEF mimicked native Ca(2+) signaling, but without preceding activation of plasma membrane receptors or channels. NsPEF stimulation may serve as a unique method to mobilize [Ca(2+)](i) and activate downstream cascades while bypassing the plasma membrane receptors.

Indexed as

AnimalsBiophysicsBuffersCalciumCalcium ChannelsCalcium SignalingCell MembraneCHO CellsCricetinaeCricetulusCytosolElectrochemistryElectroporationEndoplasmic ReticulumKineticsThapsigarginBuffersCalciumCalcium ChannelsThapsigargin

Identifiers

PMID23220180
PMCPMC3560326

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.