Evidence map›Paper›PMID 11426445›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Dissipation of potassium and proton gradients inhibits mitochondrial hyperpolarization and cytochrome c release during neural apoptosis.

M Poppe, C Reimertz, H Düssmann, A J Krohn, C M Luetjens, D Böckelmann, A L Nieminen, D Kögel, J H Prehn

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
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

30 citing papers in PubMed, 96 citations in OpenAlex.

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  11. Directed evolution of mammalian anti-apoptosis proteins by somatic hypermutation.Protein engineering, design & selection : PEDS · 2012
    Article
  12. Glutathione preconditioning ameliorates mitochondria dysfunction during warm pulmonary ischemia-reperfusion injury.European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery · 2012
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  20. Impaired mitochondria-dependent vasodilation in cerebral arteries of Zucker obese rats with insulin resistance.American journal of physiology. Regulatory, integrative and comparative physiology · 2009
    Article
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

9 authors at 2 institutions in 2 countries.

M PoppeInterdisciplinary Center for Clinical Research, Research Group "Apoptosis and Cell Death", Westphalian Wilhelms-University, D-48149 Münster, Germany.
C Reimertz
H Düssmann
A J Krohn
C M Luetjens
D Böckelmann
A L Nieminen
D Kögel
J H Prehn
Center for Clinical Research (United States) · USCase Western Reserve University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure of rat hippocampal neurons or human D283 medulloblastoma cells to the apoptosis-inducing kinase inhibitor staurosporine induced rapid cytochrome c release from mitochondria and activation of the executioner caspase-3. Measurements of cellular tetramethylrhodamine ethyl ester fluorescence and subsequent simulation of fluorescence changes based on Nernst calculations of fluorescence in the extracellular, cytoplasmic, and mitochondrial compartments revealed that the release of cytochrome c was preceded by mitochondrial hyperpolarization. Overexpression of the anti-apoptotic protein Bcl-xL, but not pharmacological blockade of outward potassium currents, inhibited staurosporine-induced hyperpolarization and apoptosis. Dissipation of mitochondrial potassium and proton gradients by valinomycin or carbonyl cyanide p-trifluoromethoxy-phenylhydrazone also potently inhibited staurosporine-induced hyperpolarization, cytochrome c release, and caspase activation. This effect was not attributable to changes in cellular ATP levels. Prolonged exposure to valinomycin induced significant matrix swelling, and per se also caused release of cytochrome c from mitochondria. In contrast to staurosporine, however, valinomycin-induced cytochrome c release and cell death were not associated with caspase-3 activation and insensitive to Bcl-xL overexpression. Our data suggest two distinct mechanisms for mitochondrial cytochrome c release: (1) active cytochrome c release associated with early mitochondrial hyperpolarization, leading to neuronal apoptosis, and (2) passive cytochrome c release secondary to mitochondrial depolarization and matrix swelling.

Indexed as

ApoptosisAnimalsbcl-X ProteinCaspase 3CaspasesCells, CulturedCytochrome c GroupEnzyme InhibitorsFluorescent DyesHippocampusImmunohistochemistryIonophoresMedulloblastomaMitochondriaNeuronsPotassiumBcl2l1 protein, ratbcl-X ProteinCASP3 protein, humanCasp3 protein, ratCaspase 3CaspasesCytochrome c GroupEnzyme InhibitorsFluorescent DyesIonophoresPotassiumProtonsProto-Oncogene Proteins c-bcl-2StaurosporineValinomycin

Identifiers

PMID11426445
PMCPMC6762374
OpenAlexW1482216160

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.