Evidence map›Paper›PMID 24978108›Full record

ArticleBiochimica et biophysica acta2014

Calcium-mediated pore expansion and cell death following nanoelectroporation.

Olga N Pakhomova, Betsy Gregory, Iurii Semenov, Andrei G Pakhomov

Abstract read
In one paragraph

Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
–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

49 citing papers in PubMed.

  1. Coronary Spasm Due to Pulsed Field Ablation: A State-of-the-Art Review.Pacing and clinical electrophysiology : PACE · 2026
    Review
  2. Article
  3. Article
  4. Impact of pulse duration on cardiac electroporation: nanosecond pulses enhance cardiomyocyte selectivity and promote a Raman-detected shift towards apoptotic cell death.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 · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Modulating CaBiophysical journal · 2024
    Article
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  10. Article
  11. Article
  12. Article
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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

4 authors.

Olga N PakhomovaFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA, USA. Electronic address: opakhomo@odu.edu.
Betsy GregoryFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA, USA.
Iurii SemenovFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA, USA.
Andrei G PakhomovFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA, USA.

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

Opening of long-lived pores in the cell membrane is the principal primary effect of intense, nanosecond pulsed electric field (nsPEF). Here we demonstrate that the evolution of pores, cell survival, the time and the mode of cell death (necrotic or apoptotic) are determined by the level of external Ca(2+) after nsPEF. We also introduce a novel, minimally disruptive technique for nsEP exposure of adherent cells on indium tin oxide (ITO)-coated glass coverslips, which does not require cell detachment and enables fast exchanges of bath media. Increasing the Ca(2+) level from the nominal 2-5μM to 2mM for the first 60-90min after permeabilization by 300-nsPEF increased the early (necrotic) death in U937, CHO, and BPAE cells. With nominal Ca(2+), the inhibition of osmotic swelling rescued cells from the early necrosis and increased caspase 3/7 activation later on. However, the inhibition of swelling had a modest or no protective effect with 2mM Ca(2+) in the medium. With the nominal Ca(2+), most cells displayed gradual increase in YO-PRO-1 and propidium (Pr) uptake. With 2mM Ca(2+), the initially lower Pr uptake was eventually replaced by a massive and abrupt Pr entry (necrotic death). It was accompanied by a transient acceleration of the growth of membrane blebs due to the increase of the intracellular osmotic pressure. We conclude that the high-Ca(2+)-dependent necrotic death in nsPEF-treated cells is effected by a delayed, sudden, and osmotically-independent pore expansion (or de novo formation of larger pores), but not by the membrane rupture.

Indexed as

ElectroporationOsmotic PressureAnimalsCalciumCaspase 3Caspase 7CattleCHO CellsCricetinaeCricetulusHumansNecrosisU937 CellsCalciumCASP3 protein, humanCASP7 protein, humanCaspase 3Caspase 7ApoptosisCalciumElectropermeabilizationElectroporationNanosecond pulseNecrosis

Identifiers

PMID24978108
PMCPMC4125538

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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.