ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2014
Microglia is a key player in the reduction of stroke damage promoted by the new antithrombotic agent ticagrelor.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.
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Who cites it
47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 83 citations in OpenAlex.
- Role and Mechanism of Microglia in White Matter Injury Recovery in Ischemic Stroke.Immunity, inflammation and disease · 2025Pooled it
- The role of convergent ion channel pathways in microglial phenotypes: a systematic review of the implications for neurological and psychiatric disorders.Translational psychiatry · 2018Pooled it
- The axon initial segment-associated microglia regulate neuronal activity and visual perception.Cell research · 2026Article
- Role of Thrombosis in Neurodegenerative Diseases: An Intricate Mechanism of Neurovascular Complications.Molecular neurobiology · 2025Review
- Clopidogrel Administration Impairs Post-Stroke Learning and Memory Recovery in Mice.International journal of molecular sciences · 2023Article
- The role of the ATP-adenosine axis in ischemic stroke.Seminars in immunopathology · 2023Review
- The Implications of Microglial Regulation in Neuroplasticity-Dependent Stroke Recovery.Biomolecules · 2023Review
- Friends or foes: The mononuclear phagocyte system in ischemic stroke.Brain pathology (Zurich, Switzerland) · 2023Review
- Ticagrelor Can Regulate the Ion Channel Characteristics of Superior Cervical Ganglion Neurons after Myocardial Infarction.Journal of cardiovascular development and disease · 2023Article
- Increased expression of the P2YRenal failure · 2023Article
- Long-term microglial phase-specific dynamics during single vessel occlusion and recanalization.Communications biology · 2022Article
- Role of NaJournal of molecular medicine (Berlin, Germany) · 2022Review
- Microglia-mediated neuroinflammation and neuroplasticity after stroke.Frontiers in cellular neuroscience · 2022Review
- The Translational Potential of Microglia and Monocyte-Derived Macrophages in Ischemic Stroke.Frontiers in immunology · 2022Review
- P2Y12 receptor as a new target for electroacupuncture relieving comorbidity of visceral pain and depression of inflammatory bowel disease.Chinese medicine · 2021Article
- Specific depletion of resident microglia in the early stage of stroke reduces cerebral ischemic damage.Journal of neuroinflammation · 2021Article
- Microglia and Neuroinflammation: What Place for P2RY12?International journal of molecular sciences · 2021Review
- Review
- Immune Cells in the BBB Disruption After Acute Ischemic Stroke: Targets for Immune Therapy?Frontiers in immunology · 2021Review
- Effects of Microglial Activation and Polarization on Brain Injury After Stroke.Frontiers in neurology · 2021Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ADP-responsive P2Y12 receptor is expressed on both platelets and microglia. Clinical data show that ticagrelor, a direct-acting, reversibly binding P2Y12-receptor antagonist, reduces total cardiovascular events, including stroke. In our present study, we investigated the expression of P2Y12 receptors and the effects of ticagrelor on brain injury in Sprague-Dawley rats subjected to a permanent middle cerebral artery occlusion (MCAo). Rats were treated per os with ticagrelor 3 mg/kg or vehicle at 10 minutes, 22, and 36 hours after MCAo and killed after 48 hours. Immunofluorescence analysis showed an ischemia-related modulation of the P2Y12 receptor, which is constitutively expressed in Iba1(+) resting microglia. After MCAo, activated microglia was mainly concentrated around the lesion, with fewer cells present inside the ischemic core. Ticagrelor significantly attenuated the evolution of ischemic damage-evaluated by magnetic resonance imaging (MRI) at 2, 24, and 48 hours after MCAo-, the number of infiltrating cells expressing the microglia/monocyte marker ED-1, the cerebral expression of proinflammatory mediators (interleukin 1 (IL-1), monocyte chemoattractant protein 1 (MCP-1), nitric oxide synthase (iNOS)) and the associated neurologic impairment. In transgenic fluorescent reporter CX3CR1-green fluorescent protein (GFP) mice, 72 hours after MCAo, ticagrelor markedly reduced GFP(+) microglia and both early and late infiltrating blood-borne cells. Finally, in primary cultured microglia, ticagrelor fully inhibited ADP-induced chemotaxis (P<0.01). Our results show that ticagrelor is protective against ischemia-induced cerebral injury and this effect is mediated, at least partly, by inhibition of P2Y12-mediated microglia activation and chemotaxis.
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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.