ArticlePloS one2010
Purinergic receptor stimulation reduces cytotoxic edema and brain infarcts in mouse induced by photothrombosis by energizing glial mitochondria.
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 38 papers.
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Who cites it
38 citing papers in PubMed, 68 citations in OpenAlex.
- The long march towards testing the adenosine receptor agonism hypothesis for human cerebroprotection: The story of the APurinergic signalling · 2026Review
- Advancing stroke recovery: unlocking the potential of cellular dynamics in stroke recovery.Cell death discovery · 2024Review
- Astrocyte-Microglia Crosstalk: A Novel Target for the Treatment of Migraine.Aging and disease · 2024Review
- P2Y1 Receptor as a Catalyst of Brain Neurodegeneration.NeuroSci · 2022Review
- Selective Ablation ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Protective Effects of ShcA Protein Silencing for Photothrombotic Cerebral Infarction.Translational stroke research · 2021Article
- Neurovascular Unit: A critical role in ischemic stroke.CNS neuroscience & therapeutics · 2021Review
- Glial Cells: Role of the Immune Response in Ischemic Stroke.Frontiers in immunology · 2020Review
- Neuroprotective effects of microglial P2YJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Time to Target Stroke: Examining the Circadian System in Stroke.The Yale journal of biology and medicine · 2019Review
- HIV-1 Tat enhances purinergic P2Y4 receptor signaling to mediate inflammatory cytokine production and neuronal damage via PI3K/Akt and ERK MAPK pathways.Journal of neuroinflammation · 2019Article
- Mitochondrial Dysfunction in Stroke: Implications of Stem Cell Therapy.Translational stroke research · 2018Review
- Insulin-like growth factor receptor signaling regulates working memory, mitochondrial metabolism, and amyloid-β uptake in astrocytes.Molecular metabolism · 2018Article
- Detection, risk factors, and functional consequences of cerebral microinfarcts.The Lancet. Neurology · 2017Review
- Stimulation of astrocyte fatty acid oxidation by thyroid hormone is protective against ischemic stroke-induced damage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Glutamate and ATP at the Interface Between Signaling and Metabolism in Astroglia: Examples from Pathology.Neurochemical research · 2017Review
- Glycolysis and oxidative phosphorylation are essential for purinergic receptor-mediated angiogenic responses in vasa vasorum endothelial cells.American journal of physiology. Cell physiology · 2017Article
- Sex differences in astrocyte and microglia responses immediately following middle cerebral artery occlusion in adult mice.Neuroscience · 2016Article
- Calcineurin β protects brain after injury by activating the unfolded protein response.Neurobiology of disease · 2016Article
- Astrocytes, therapeutic targets for neuroprotection and neurorestoration in ischemic stroke.Progress in neurobiology · 2016Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Treatments to improve the neurological outcome of edema and cerebral ischemic stroke are severely limited. Here, we present the first in vivo single cell images of cortical mouse astrocytes documenting the impact of single vessel photothrombosis on cytotoxic edema and cerebral infarcts. The volume of astrocytes expressing green fluorescent protein (GFP) increased by over 600% within 3 hours of ischemia. The subsequent growth of cerebral infarcts was easily followed as the loss of GFP fluorescence as astrocytes lysed. Cytotoxic edema and the magnitude of ischemic lesions were significantly reduced by treatment with the purinergic ligand 2-methylthioladenosine 5' diphosphate (2-MeSADP), an agonist with high specificity for the purinergic receptor type 1 isoform (P2Y(1)R). At 24 hours, cytotoxic edema in astrocytes was still apparent at the penumbra and preceded the cell lysis that defined the infarct. Delayed 2MeSADP treatment, 24 hours after the initial thrombosis, also significantly reduced cytotoxic edema and the continued growth of the brain infarction. Pharmacological and genetic evidence are presented indicating that 2MeSADP protection is mediated by enhanced astrocyte mitochondrial metabolism via increased inositol trisphosphate (IP(3))-dependent Ca(2+) release. We suggest that mitochondria play a critical role in astrocyte energy metabolism in the penumbra of ischemic lesions, where low ATP levels are widely accepted to be responsible for cytotoxic edema. Enhancement of this energy source could have similar protective benefits for a wide range of brain injuries.
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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.