ArticlePloS one2010
Anthrax lethal toxin suppresses murine cardiomyocyte contractile function and intracellular Ca2+ handling via a NADPH oxidase-dependent mechanism.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Innate Immune Receptors, Key Actors in Cardiovascular Diseases.JACC. Basic to translational science · 2020Review
- Identification of a Substrate-selective Exosite within the Metalloproteinase Anthrax Lethal Factor.The Journal of biological chemistry · 2017Article
- Profiling lethal factor interacting proteins from human stomach using T7 phage display screening.Molecular medicine reports · 2016Article
- Review
- Review
- B. anthracis associated cardiovascular dysfunction and shock: the potential contribution of both non-toxin and toxin components.BMC medicine · 2013Review
- Activated protein C ameliorates Bacillus anthracis lethal toxin-induced lethal pathogenesis in rats.Journal of biomedical science · 2012Article
- Cardiac-specific catalase overexpression rescues anthrax lethal toxin-induced cardiac contractile dysfunction: role of oxidative stress and autophagy.BMC medicine · 2012Article
- Toll-like receptor 4 knockout protects against anthrax lethal toxin-induced cardiac contractile dysfunction: role of autophagy.British journal of pharmacology · 2012Article
- Facilitated ethanol metabolism promotes cardiomyocyte contractile dysfunction through autophagy in murine hearts.Autophagy · 2012Article
- Protective antigen antibody augments hemodynamic support in anthrax lethal toxin shock in canines.The Journal of infectious diseases · 2012Article
- New insights into the biological effects of anthrax toxins: linking cellular to organismal responses.Microbes and infection · 2012Review
- Cellular and physiological effects of anthrax exotoxin and its relevance to disease.Frontiers in cellular and infection microbiology · 2012Review
- Anthrax infection.American journal of respiratory and critical care medicine · 2011Review
- AMP-dependent kinase and autophagic flux are involved in aldehyde dehydrogenase-2-induced protection against cardiac toxicity of ethanol.Free radical biology & medicine · 2011Article
- The potential contributions of lethal and edema toxins to the pathogenesis of anthrax associated shock.Toxins · 2011Review
- Anthrax edema toxin has cAMP-mediated stimulatory effects and high-dose lethal toxin has depressant effects in an isolated perfused rat heart model.American journal of physiology. Heart and circulatory physiology · 2011Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesAnthrax infection is associated with devastating cardiovascular sequelae, suggesting unfavorable cardiovascular effects of toxins originated from Bacillus anthracis namely lethal and edema toxins. This study was designed to examine the direct effect of lethal toxins on cardiomyocyte contractile and intracellular Ca(2+) properties.
methodsMurine cardiomyocyte contractile function and intracellular Ca(2+) handling were evaluated including peak shortening (PS), maximal velocity of shortening/ relengthening (± dL/dt), time-to-PS (TPS), time-to-90% relengthening (TR(90)), intracellular Ca(2+) rise measured as fura-2 fluorescent intensity (ΔFFI), and intracellular Ca(2+) decay rate. Stress signaling and Ca(2+) regulatory proteins were assessed using Western blot analysis.
resultsIn vitro exposure to a lethal toxin (0.05-50 nM) elicited a concentration-dependent depression on cardiomyocyte contractile and intracellular Ca(2+) properties (PS, ± dL/dt, ΔFFI), along with prolonged duration of contraction and intracellular Ca(2+) decay, the effects of which were nullified by the NADPH oxidase inhibitor apocynin. The lethal toxin significantly enhanced superoxide production and cell death, which were reversed by apocynin. In vivo lethal toxin exposure exerted similar time-dependent cardiomyocyte mechanical and intracellular Ca(2+) responses. Stress signaling cascades including MEK1/2, p38, ERK and JNK were unaffected by in vitro lethal toxins whereas they were significantly altered by in vivo lethal toxins. Ca(2+) regulatory proteins SERCA2a and phospholamban were also differentially regulated by in vitro and in vivo lethal toxins. Autophagy was drastically triggered although ER stress was minimally affected following lethal toxin exposure.
conclusionsOur findings indicate that lethal toxins directly compromised murine cardiomyocyte contractile function and intracellular Ca(2+) through a NADPH oxidase-dependent mechanism.
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Registered trials
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.