ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2017
Augmentation of poly(ADP-ribose) polymerase-dependent neuronal cell death by acidosis.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 28 citations in OpenAlex.
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- Sex-dependent role of 20-HETE synthesis in outcome from ischemic stroke in rats.Physiological reports · 2026Article
- Targeting DNA Damage and Repair Pathways in Cerebral Ischemic Stroke: From Bench to Bedside.Translational stroke research · 2026Review
- Oxidative stress as a driver of organelle cascade damage in neurological diseases.Frontiers in aging neuroscience · 2026Review
- Multicenter Stroke Preclinical Assessment Network Analysis of Cardiovascular Risk Factor Subgroups Treated With the Poly(ADP-Ribose) Polymerase Inhibitor Veliparib.Journal of the American Heart Association · 2025Article
- The Impact of Calcium Overload on Cellular Processes: Exploring Calcicoptosis and Its Therapeutic Potential in Cancer.International journal of molecular sciences · 2024Review
- Ozone therapy mitigates parthanatos after ischemic stroke.Biological research · 2024Article
- Blood glucose to predict symptomatic intracranial hemorrhage after endovascular treatment of acute ischemic stroke with large infarct core: a prospective observational study.Frontiers in neurology · 2024Article
- Application of stimuli-responsive nanomedicines for the treatment of ischemic stroke.Frontiers in bioengineering and biotechnology · 2023Review
- Fasting blood glucose as a predictor of progressive infarction in men with acute ischemic stroke.The Journal of international medical research · 2022Article
- Modes of Brain Cell Death Following Intracerebral Hemorrhage.Frontiers in cellular neuroscience · 2022Review
- Microglia-derived interleukin-10 accelerates post-intracerebral hemorrhage hematoma clearance by regulating CD36.Brain, behavior, and immunity · 2021Article
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- Recent advances in preventing neurodegenerative diseases.Faculty reviews · 2021Review
- Targeting Parthanatos in Ischemic Stroke.Frontiers in neurology · 2021Review
- The Female Impact in the World of Neurodegeneration.Frontiers in integrative neuroscience · 2021Article
- Overexpression of apoptosis inducing factor aggravates hypoxic-ischemic brain injury in neonatal mice.Cell death & disease · 2020Article
- Sulforaphane Protects Piglet Brains from Neonatal Hypoxic-Ischemic Injury.Developmental neuroscience · 2020Article
- Admission Glucose Levels May Increase the Risk for Early Neurological Deterioration in Females With Acute Ischemic Stroke.Frontiers in neurology · 2020Article
- Microglial Depletion with Clodronate Liposomes Increases Proinflammatory Cytokine Levels, Induces Astrocyte Activation, and Damages Blood Vessel Integrity.Molecular neurobiology · 2019Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Tissue acidosis is a key component of cerebral ischemic injury, but its influence on cell death signaling pathways is not well defined. One such pathway is parthanatos, in which oxidative damage to DNA results in activation of poly(ADP-ribose) polymerase and generation of poly(ADP-ribose) polymers that trigger release of mitochondrial apoptosis-inducing factor. In primary neuronal cultures, we first investigated whether acidosis per sé is capable of augmenting parthanatos signaling initiated pharmacologically with the DNA alkylating agent, N-methyl- N'-nitro- N-nitrosoguanidine. Exposure of neurons to medium at pH 6.2 for 4 h after N-methyl- N'-nitro- N-nitrosoguanidine washout increased intracellular calcium and augmented the N-methyl- N'-nitro- N-nitrosoguanidine-evoked increase in poly(ADP-ribose) polymers, nuclear apoptosis-inducing factor , and cell death. The augmented nuclear apoptosis-inducing factor and cell death were blocked by the acid-sensitive ion channel-1a inhibitor, psalmotoxin. In vivo, acute hyperglycemia during transient focal cerebral ischemia augmented tissue acidosis, poly(ADP-ribose) polymers formation, and nuclear apoptosis-inducing factor , which was attenuated by a poly(ADP-ribose) polymerase inhibitor. Infarct volume from hyperglycemic ischemia was decreased in poly(ADP-ribose) polymerase 1-null mice. Collectively, these results demonstrate that acidosis can directly amplify neuronal parthanatos in the absence of ischemia through acid-sensitive ion channel-1a . The results further support parthanatos as one of the mechanisms by which ischemia-associated tissue acidosis augments cell death.
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