biostudies-literatureSladojevic NNational Institute for General Medical ScienceNational Institute of Neurological Disorders and StrokeNHLBI NIH HHSNINDS NIH HHSNIGMS NIH HHS57-70https://www.ebi.ac.uk/biostudies/studies/S-EPMC4273560biostudies-literatureUnknown67Proinflammatory 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-ApNeurobiology of diseaseInhibition of junctional adhesion molecule-A/LFA interaction attenuates leukocyte trafficking and inflammation in brain ischemia/reperfusion injury.PMC4273560T32 HL007517R01 NS062853NS034709R01 GM029507R01 NS034709GM29507NS062853R37 GM029507GM61656R56 NS062853R01 GM061656Keep RFSladojevic NSarma JVStamatovic SMGrailer JJWard PAAndjelkovic AVfalseInhibition of junctional adhesion molecule-A/LFA interaction attenuates leukocyte trafficking and inflammation in brain ischemia/reperfusion injury.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-Ap2014-01-01T00:00:00Z2014 Jul2025-04-19T14:41:22.84Z2019-03-27T01:42:12ZS-EPMC42735602465791910.1016/j.nbd.2014.03.010