ArticleASN neuro
Prostaglandin E2 EP2 receptor deletion attenuates intracerebral hemorrhage-induced brain injury and improves functional recovery.
Article in ASN neuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- A transcriptomic analysis of cerebral microvessels reveals the involvement of Notch1 signaling in endothelial mitochondrial-dysfunction-dependent BBB disruption.Fluids and barriers of the CNS · 2022Article
- Targeting gliovascular connexins prevents inflammatory blood-brain barrier leakage and astrogliosis.JCI insight · 2022Article
- International Union of Basic and Clinical Pharmacology. CIX. Differences and Similarities between Human and Rodent Prostaglandin EPharmacological reviews · 2020Article
- Role of the PGECNS neuroscience & therapeutics · 2020Article
- Targeting prostaglandin receptor EP2 for adjunctive treatment of status epilepticus.Pharmacology & therapeutics · 2020Review
- Prostaglandin EJournal of the American Heart Association · 2018Article
- Increased brain hemopexin levels improve outcomes after intracerebral hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Article
- Discovery of 2-Piperidinyl Phenyl Benzamides and Trisubstituted Pyrimidines as Positive Allosteric Modulators of the Prostaglandin Receptor EP2.ACS chemical neuroscience · 2018Article
- The absence of the CD163 receptor has distinct temporal influences on intracerebral hemorrhage outcomes.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Article
- Genetic Deletion of PGFFrontiers in neuroscience · 2018Article
- Insulin-like Growth Factor Binding Protein6 Associated with Neuronal Apoptosis Following Intracerebral Hemorrhage in Rats.Cellular and molecular neurobiology · 2017Article
- Connexin Channels at the Glio-Vascular Interface: Gatekeepers of the Brain.Neurochemical research · 2017Review
- Increased Expression of Ubiquitin-Specific Protease 4 Participates in Neuronal Apoptosis After Intracerebral Hemorrhage in Adult Rats.Cellular and molecular neurobiology · 2017Article
- Hck Promotes Neuronal Apoptosis Following Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2017Article
- Resveratrol Attenuates Neurodegeneration and Improves Neurological Outcomes after Intracerebral Hemorrhage in Mice.Frontiers in cellular neuroscience · 2017Article
- Cerebroprotection by the neuronal PGE2 receptor EP2 after intracerebral hemorrhage in middle-aged mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- PGE2-EP3 signaling exacerbates intracerebral hemorrhage outcomes in 24-mo-old mice.American journal of physiology. Heart and circulatory physiology · 2016Article
- Defining the therapeutic time window for suppressing the inflammatory prostaglandin E2 signaling after status epilepticus.Expert review of neurotherapeutics · 2016Review
- MicroRNA367 negatively regulates the inflammatory response of microglia by targeting IRAK4 in intracerebral hemorrhage.Journal of neuroinflammation · 2015Article
- Targeting brain microvascular endothelial cells: a therapeutic approach to neuroprotection against stroke.Neural regeneration research · 2015Review
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Intracerebral hemorrhage (ICH) is a devastating type of stroke characterized by bleeding into the brain parenchyma and secondary brain injury resulting from strong neuroinflammatory responses to blood components. Production of prostaglandin E2 (PGE2) is significantly upregulated following ICH and contributes to this inflammatory response in part through its E prostanoid receptor subtype 2 (EP2). Signaling through the EP2 receptor has been shown to affect outcomes of many acute and chronic neurological disorders; although, not yet explored in the context of ICH. Wildtype (WT) and EP2 receptor knockout (EP2(-/-)) mice were subjected to ICH, and various anatomical and functional outcomes were assessed by histology and neurobehavioral testing, respectively. When compared with age-matched WT controls, EP2(-/-) mice had 41.9 ± 4.7% smaller ICH-induced brain lesions and displayed significantly less ipsilateral hemispheric enlargement and incidence of intraventricular hemorrhage. Anatomical outcomes correlated with improved functional recovery as identified by neurological deficit scoring. Histological staining was performed to begin investigating the mechanisms involved in EP2-mediated neurotoxicity after ICH. EP2(-/-) mice exhibited 45.5 ± 5.8% and 41.4 ± 8.1% less blood and ferric iron accumulation, respectively. Furthermore, significantly less striatal and cortical microgliosis, striatal and cortical astrogliosis, blood-brain barrier breakdown, and peripheral neutrophil infiltration were seen in EP2(-/-) mice. This study is the first to suggest a deleterious role for the PGE2-EP2 signaling axis in modulating brain injury, inflammation, and functional recovery following ICH. Targeting the EP2 G protein-coupled receptor may represent a new therapeutic avenue for the treatment of hemorrhagic stroke.
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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.