title: Overexpression of monocyte chemoattractant protein 1 in the brain exacerbates ischemic brain injury and is associated with recruitment of inflammatory cells.
abstract: Brain cells produce cytokines and chemokines during the inflammatory process after stroke both in animal models and in patients. Monocyte chemoattractant protein 1 (MCP-1), one of the proinflammatory chemokines, can attract monocytes to the tissue where MCP-1 is overexpressed. However, the role of MCP-1 elevation in stroke has not been explored in detail. The authors hypothesized that elevated MCP-1 levels would lead to increased influx of monocytes and increased brain infarction size in stroke induced by middle cerebral artery occlusion with partial reperfusion. There were no differences in blood pressure, blood flow, or vascular architecture between wild-type mice and transgenic MBP-JE mice. Twenty-four to 48 hours after middle cerebral artery occlusion, brain infarction volumes after ischemia were significantly larger in MBP-JE mice than in wild-type controls and were accompanied by increased local transmigration and perivascular accumulation of macrophages and neutrophils. These results indicate that MCP-1 can contribute to inflammatory injury in stroke.
authors.affiliation: Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-4128, USA.
authors.forename: Yong
authors.initials: Y
authors.lastname: Chen
authors.forename: John M
authors.initials: JM
authors.lastname: Hallenbeck
authors.forename: Christl
authors.initials: C
authors.lastname: Ruetzler
authors.forename: David
authors.initials: D
authors.lastname: Bol
authors.forename: Karen
authors.initials: K
authors.lastname: Thomas
authors.forename: Nancy E J
authors.initials: NE
authors.lastname: Berman
authors.forename: Stefanie N
authors.initials: SN
authors.lastname: Vogel
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001921:Brain / Q000276:immunology / Q000473:pathology; D002560:Cerebrovascular Circulation; D018932:Chemokine CCL2 / Q000235:genetics*; D002941:Circle of Willis / Q000033:anatomy & histology; D004195:Disease Models, Animal; D005260:Female; D015870:Gene Expression / Q000276:immunology; D020244:Infarction, Middle Cerebral Artery / Q000276:immunology / Q000473:pathology*; D002546:Ischemic Attack, Transient / Q000276:immunology / Q000473:pathology*; D008264:Macrophages / Q000276:immunology / Q000473:pathology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D008822:Mice, Transgenic; D020768:Middle Cerebral Artery / Q000033:anatomy & histology; D009000:Monocytes / Q000276:immunology / Q000473:pathology; D009504:Neutrophils / Q000276:immunology / Q000473:pathology*; D015427:Reperfusion Injury / Q000276:immunology / Q000473:pathology
chemical_list: D018932:Chemokine CCL2