ArticleMedical molecular morphology2009
Unique mode of cell death in freshly isolated adult rat ventricular cardiomyocytes exposed to hydrogen peroxide.
Article in Medical molecular morphology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Ischaemic Preconditioning Protects Cardiomyocytes from Anthracycline-Induced Toxicity via the PI3K Pathway.Cardiovascular drugs and therapy · 2018Article
- Overexpression of Twinkle-helicase protects cardiomyocytes from genotoxic stress caused by reactive oxygen species.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Neuregulin-1 suppresses cardiomyocyte apoptosis by activating PI3K/Akt and inhibiting mitochondrial permeability transition pore.Molecular and cellular biochemistry · 2012Article
- Cardiomyocyte deletion of mitofusin-1 leads to mitochondrial fragmentation and improves tolerance to ROS-induced mitochondrial dysfunction and cell death.American journal of physiology. Heart and circulatory physiology · 2012Article
- Apoptotic effects of hydrogen peroxide and vitamin C on chicken embryonic fibroblasts: redox state and programmed cell death.Cytotechnology · 2011Article
- Early long-term L-T3 replacement rescues mitochondria and prevents ischemic cardiac remodelling in rats.Journal of cellular and molecular medicine · 2011Article
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To address whether adult rat ventricular cardiomyocytes (ARVCs) exposed to oxidant stress die via apoptosis (secondarily by necrosis) or primarily by necrosis, we exposed ARVCs to hydrogen peroxide (H2O2; 0.1-100 microM) for up to 24 h and then compared them with isoproterenol-induced apoptotic and Triton X-induced necrotic controls. Cellular shrinkage preceded plasma membrane disruption, reflected by trypan blue uptake in ARVCs exposed to lower concentrations of H2O2 (<1 microM; an apoptotic pattern), but the order was reversed in cells exposed to higher concentrations of H2O2 (>1 microM; a necrotic pattern). DNA fragmentation, caspase-3 activation, mitochondrial membrane potential preservation, and ATP preservation were all apparent in ARVCs treated with low H2O2 (0.5 microM), but not in those treated with high H2O2 (10 microM). In addition, electron microscopy revealed unique morphology in H2O2-treated ARVCs; i.e., the nuclei had a homogeneous ground glass-like appearance that was never accompanied by chromatin condensation. Apparently, high concentrations of H2O2 caused primary necrosis in ARVCs, whereas low concentrations induced biochemically comparable apoptosis, although the latter did not satisfy the morphological criteria of apoptosis. These findings caution against the use of oxidant stress, H2O2 in particular, as an inducer of apoptosis in ARVCs.
Indexed as
Identifiers
19536616What 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.