ArticleCellular and molecular life sciences : CMLS2009
Oxidative stress triggers neuronal caspase-independent death: endonuclease G involvement in programmed cell death-type III.
Article in Cellular and molecular life sciences : CMLS, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- Nuclear endonuclease G controls cell proliferation in ovarian cancer.FEBS open bio · 2023Article
- Apoptotic effects of3 Biotech · 2023Article
- PHLPP Inhibitor NSC74429 Is Neuroprotective in Rodent Models of Cardiac Arrest and Traumatic Brain Injury.Biomolecules · 2022Article
- VDAC1 regulates neuronal cell loss after retinal trauma injury by a mitochondria-independent pathway.Cell death & disease · 2022Article
- Picroside II Exerts a Neuroprotective Effect by Inhibiting mPTP Permeability and EndoG Release after Cerebral Ischemia/Reperfusion Injury in Rats.Journal of molecular neuroscience : MN · 2018Article
- Repeated Mild Traumatic Brain Injury: Potential Mechanisms of Damage.Cell transplantation · 2017Review
- Cold-inducible RNA-binding protein through TLR4 signaling induces mitochondrial DNA fragmentation and regulates macrophage cell death after trauma.Cell death & disease · 2017Article
- Intracerebral Hemorrhage, Oxidative Stress, and Antioxidant Therapy.Oxidative medicine and cellular longevity · 2016Review
- PPARα activation attenuates amyloid-β-dependent neurodegeneration by modulating Endo G and AIF translocation.Neurotoxicity research · 2015Article
- Involvement of hydrogen peroxide in safingol-induced endonuclease G-mediated apoptosis of squamous cell carcinoma cells.International journal of molecular sciences · 2014Article
- Endonuclease-G and the pathways to dopaminergic neurodegeneration: a question of location?The EMBO journal · 2013Article
- CHIP has a protective role against oxidative stress-induced cell death through specific regulation of endonuclease G.Cell death & disease · 2013Article
- Mouse embryonic stem cells undergo charontosis, a novel programmed cell death pathway dependent upon cathepsins, p53, and EndoG, in response to etoposide treatment.Stem cell research · 2013Article
- AIF, reactive oxygen species, and neurodegeneration: a "complex" problem.Neurochemistry international · 2013Review
- Phanta: a non-fluorescent photochromic acceptor for pcFRET.PloS one · 2013Article
- Exposure to ionizing radiation induced persistent gene expression changes in mouse mammary gland.Radiation oncology (London, England) · 2012Article
- Article
- Autophagic activity in cortical neurons under acute oxidative stress directly contributes to cell death.Cellular and molecular life sciences : CMLS · 2011Article
- Endonuclease G does not play an obligatory role in poly(ADP-ribose) polymerase-dependent cell death after transient focal cerebral ischemia.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Article
- Basic mechanisms of neurodegeneration: a critical update.Journal of cellular and molecular medicine · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To characterize neuronal death, primary cortical neurons (C57/Black 6 J mice) were exposed to hydrogen peroxide (H2O2) and staurosporine. Both caused cell shrinkage, nuclear condensation, DNA fragmentation and loss of plasma membrane integrity. Neither treatment induced caspase-7 activity, but caspase-3 was activated by staurosporine but not H2O2. Each treatment caused redistribution from mitochondria of both endonuclease G (Endo G) and cytochrome c. Neurons knocked down for Endo G expression using siRNA showed reduction in both nuclear condensation and DNA fragmentation after treatment with H2O2, but not staurosporine. Endo G suppression protected cells against H2O2-induced cell death, while staurosporine-induced death was merely delayed. We conclude that staurosporine induces apoptosis in these neurons, but severe oxidative stress leads to Endo G-dependent death, in the absence of caspase activation (programmed cell death-type III). Therefore, oxidative stress triggers in neurons a form of necrosis that is a systematic cellular response subject to molecular regulation.
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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.