Evidence map›Paper›PMID 25243426›Full record

ArticleShock (Augusta, Ga.)2015

Cardiac myocyte dysfunction induced by streptolysin O is membrane pore and calcium dependent.

Devin D Bolz, Zhi Li, Eric R McIndoo, Rodney K Tweten, Amy E Bryant, Dennis L Stevens

Open access · greenAbstract read
In one paragraph

Article in Shock (Augusta, Ga.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  13. [Atrial fibrillation in patients with sepsis and non-cardiac infections].Herzschrittmachertherapie & Elektrophysiologie · 2019
    Review
  14. Article
  15. Review
  16. Cell-penetrating peptides derived fromThe Journal of biological chemistry · 2018
    Article
  17. 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

6 authors at 2 institutions in 1 country.

Devin D Bolz*Infectious Diseases Section, Department of Veterans Affairs Medical Center, Boise, Idaho; †Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; ‡University of Washington School of Medicine, Seattle, Washington.
Zhi Li
Eric R McIndoo
Rodney K Tweten
Amy E Bryant
Dennis L Stevens
University of Washington · USUniversity of Oklahoma Health Sciences Center · US

Funding

Women's health: interplay of maternal diet and key demographics on neurological health in the rural frontier and remote WestP20GM103408 · NIGMS · UNIVERSITY OF IDAHO · PI Carolyn Hovde Bohach · 2012 to 2026
$59.8M
Pore Formation by Cholesterol Dependent CytolysinsR01AI037657 · NIAID · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI TWETEN, RODNEY K. · 1997 to 2015
$5.4M
Cardiac dysfunction in StrepTSS: interplay of SLO and MMPsI01BX001726 · VA · BOISE VA MEDICAL CENTER · PI STEVENS, DENNIS L · 2013 to 2016
–
BLRD VA I01 BX001726NIAID NIH HHS R01 AI037657NIGMS NIH HHS P20 GM103408
6 · The paper itself

Abstract

Septic cardiomyopathy is a severe complication among some patients who develop group A streptococcal toxic shock syndrome. Despite the importance of cardiac dysfunction in determining prognosis, very little is known about mechanisms that reduce cardiac output in association with streptococcal infection. Here, we investigated the effects of streptococcal extracellular toxins on mechanical contractility of electrically paced primary murine cardiomyocytes. Our data demonstrate that streptolysin O (SLO) is the major streptococcal toxin responsible for cardiomyocyte contractile dysfunction. Streptolysin O dose-dependently affected cardiac myocyte function in discrete stages. Exposure to SLO caused a failure of cardiac cells to respond to electrical pacing, followed by spontaneous dysregulated contractions and augmented strength of contraction. Central to these SLO-mediated effects is a marked influx of calcium into the cytosol through SLO-mediated pores in the cytoplasmic membrane. Such calcium mobilization in response to SLO correlated temporally with hypercontractility and unpaced contractions. During continued exposure to SLO, cardiomyocytes exhibited periods of reversion to normal electrical pacing suggestive of membrane lesion repair and restoration of calcium handling. Together, these observations are consistent with the clinical observation that septic cardiomyopathy is a reversible condition in patients who survive streptococcal toxic shock syndrome. These data provide strong evidence that streptococcal exotoxins, specifically SLO, can directly impact cardiac mechanical function.

Indexed as

AnimalsBacterial ProteinsCalciumCalcium ChannelsCell MembraneCell Membrane PermeabilityCells, CulturedDose-Response Relationship, DrugElectric StimulationFemaleMice, Inbred C57BLMyocardial ContractionMyocytes, CardiacStreptolysinsBacterial ProteinsCalciumCalcium Channelsstreptolysin OStreptolysins

Identifiers

PMID25243426
PMCPMC4297253
OpenAlexW2324774300

What OpenQuestion holds

Textmetadata
LicenceTDM
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.