ArticleThe American journal of pathology1997
Troponin T cross-linking in human apoptotic cardiomyocytes.
Article in The American journal of pathology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed, 35 citations in OpenAlex.
- A comprehensive review on the effects of sex hormones on chemotherapy-induced cardiotoxicity: are they lucrative or unprofitable?Cardio-oncology (London, England) · 2024Review
- Identification of cardiac myofilament protein isoforms using multiple mass spectrometry based approaches.Proteomics. Clinical applications · 2014Article
- Transcriptome transfer provides a model for understanding the phenotype of cardiomyocytes.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Nonmyofilament-associated troponin T fragments induce apoptosis.American journal of physiology. Heart and circulatory physiology · 2009Article
- Roles of transglutaminases in cardiac and vascular diseases.Frontiers in bioscience : a journal and virtual library · 2007Review
- Molecular and cellular mechanisms of cardiotoxicity.Environmental health perspectives · 2001Review
- Troponin T: genetics, properties and function.Journal of muscle research and cell motility · 1998Review
- Rabbit cardiac and skeletal myocytes differ in constitutive and inducible expression of the glucose-regulated protein GRP94.The Biochemical journal · 1998Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracellular calcium overload of guinea pig cardiomyocytes is accompanied by troponin T cross-linking, which is revealed by changes in immunoreactivity of anti-troponin T antibodies. We presently investigated whether the same process is detectable in the human heart. Immunohistochemistry shows myofibrillar staining with BN-59 anti-troponin T antibody with rare cardiomyocytes in samples obtained at surgery, whereas approximately 50% of myocytes are labeled in heart samples taken at autopsy within 3 hours of death, and every cardiomyocyte is stained after exposure of biopsy sections to 10 mmol/L calcium. Western blot analysis shows reactive polypeptides of approximately 70 and 85 to 90 kd in addition to troponin T in both treated and autopsy heart sections. Neither reactivity in immunohistochemistry nor additional reactive polypeptides in Western blot are detectable when calpain or transglutaminase is inhibited during exposure of sections to high calcium. Troponin T crosslinking occurs also in isolated myofibrils, which show staining with BN-59 at either sarcomeric A or I bands. Labeling with TdT-mediated dUTP nick and labeling (TUNEL) to demonstrate apoptosis reveals DNA fragmentation in BN-59-positive myocytes. Thus, troponin T cross-linking occurs in human cardiac myocytes concomitantly with apoptosis and autopsy autolysis, suggesting that similar cytosolic alterations can be produced by different types of myocyte death.
Indexed as
Identifiers
9176400PMC1858314W1567560709What OpenQuestion holds
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.