{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sladojevic N"],"funding":["National Institute for General Medical Science","National Institute of Neurological Disorders and Stroke","NHLBI NIH HHS","NINDS NIH HHS","NIGMS NIH HHS"],"pagination":["57-70"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4273560"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["67"],"pubmed_abstract":["Proinflammatory mediators trigger intensive postischemic inflammatory remodeling of the blood-brain barrier (BBB) including extensive brain endothelial cell surface and junctional complex changes. Junctional adhesion molecule-A (JAM-A) is a component of the brain endothelial junctional complex with dual roles: paracellular route occlusion and regulating leukocyte docking and migration. The current study examined the contribution of JAM-A to the regulation of leukocyte (neutrophils and monocytes/macrophages) infiltration and the postischemic inflammatory response in brain ischemia/reperfusion (I/R injury). Brain I/R injury was induced by transient middle cerebral artery occlusion (MCAO) for 30min in mice followed by reperfusion for 0-5days, during which time JAM-A antagonist peptide (JAM-Ap"],"journal":["Neurobiology of disease"],"pubmed_title":["Inhibition of junctional adhesion molecule-A/LFA interaction attenuates leukocyte trafficking and inflammation in brain ischemia/reperfusion injury."],"pmcid":["PMC4273560"],"funding_grant_id":["T32 HL007517","R01 NS062853","NS034709","R01 GM029507","R01 NS034709","GM29507","NS062853","R37 GM029507","GM61656","R56 NS062853","R01 GM061656"],"pubmed_authors":["Keep RF","Sladojevic N","Sarma JV","Stamatovic SM","Grailer JJ","Ward PA","Andjelkovic AV"],"additional_accession":[]},"is_claimable":false,"name":"Inhibition of junctional adhesion molecule-A/LFA interaction attenuates leukocyte trafficking and inflammation in brain ischemia/reperfusion injury.","description":"Proinflammatory mediators trigger intensive postischemic inflammatory remodeling of the blood-brain barrier (BBB) including extensive brain endothelial cell surface and junctional complex changes. Junctional adhesion molecule-A (JAM-A) is a component of the brain endothelial junctional complex with dual roles: paracellular route occlusion and regulating leukocyte docking and migration. The current study examined the contribution of JAM-A to the regulation of leukocyte (neutrophils and monocytes/macrophages) infiltration and the postischemic inflammatory response in brain ischemia/reperfusion (I/R injury). Brain I/R injury was induced by transient middle cerebral artery occlusion (MCAO) for 30min in mice followed by reperfusion for 0-5days, during which time JAM-A antagonist peptide (JAM-Ap","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Jul","modification":"2025-04-19T14:41:22.84Z","creation":"2019-03-27T01:42:12Z"},"accession":"S-EPMC4273560","cross_references":{"pubmed":["24657919"],"doi":["10.1016/j.nbd.2014.03.010"]}}