<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liang X</submitter><funding>NINDS NIH HHS</funding><pagination>4362-71</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3204834</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>121(11)</volume><pubmed_abstract>Stroke is the third leading cause of death in the United States. Fewer than 5% of patients benefit from the only intervention approved to treat stroke. Thus, there is an enormous need to identify new therapeutic targets. The role of inducible cyclooxygenase (COX-2) activity in stroke and other neurologic diseases is complex, as both activation and sustained inhibition can engender cerebral injury. Whether COX-2 induces cerebroprotective or injurious effects is probably dependent on which downstream prostaglandin receptors are activated. Here, we investigated the function of the PGE2 receptor EP4 in a mouse model of cerebral ischemia. Systemic administration of a selective EP4 agonist after ischemia reduced infarct volume and ameliorated long-term behavioral deficits. Expression of EP4 was </pubmed_abstract><journal>The Journal of clinical investigation</journal><pubmed_title>Signaling via the prostaglandin E₂ receptor EP4 exerts neuronal and vascular protection in a mouse model of cerebral ischemia.</pubmed_title><pmcid>PMC3204834</pmcid><funding_grant_id>R01 NS045727</funding_grant_id><funding_grant_id>R01NS045727</funding_grant_id><pubmed_authors>Andreasson K</pubmed_authors><pubmed_authors>Wang Q</pubmed_authors><pubmed_authors>Pan T</pubmed_authors><pubmed_authors>Liang X</pubmed_authors><pubmed_authors>Lin L</pubmed_authors><pubmed_authors>Anacker C</pubmed_authors><pubmed_authors>Merchant M</pubmed_authors><pubmed_authors>Woodling NS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Signaling via the prostaglandin E₂ receptor EP4 exerts neuronal and vascular protection in a mouse model of cerebral ischemia.</name><description>Stroke is the third leading cause of death in the United States. Fewer than 5% of patients benefit from the only intervention approved to treat stroke. Thus, there is an enormous need to identify new therapeutic targets. The role of inducible cyclooxygenase (COX-2) activity in stroke and other neurologic diseases is complex, as both activation and sustained inhibition can engender cerebral injury. Whether COX-2 induces cerebroprotective or injurious effects is probably dependent on which downstream prostaglandin receptors are activated. Here, we investigated the function of the PGE2 receptor EP4 in a mouse model of cerebral ischemia. Systemic administration of a selective EP4 agonist after ischemia reduced infarct volume and ameliorated long-term behavioral deficits. Expression of EP4 was </description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Nov</publication><modification>2025-04-04T07:25:27.158Z</modification><creation>2019-03-27T00:45:32Z</creation></dates><accession>S-EPMC3204834</accession><cross_references><pubmed>21965326</pubmed><doi>10.1172/jci46279</doi><doi>10.1172/JCI46279</doi></cross_references></HashMap>