Effect of neutrophil depletion on gelatinase expression, edema formation and hemorrhagic transformation after focal ischemic stroke.

Hdl Handle:
http://hdl.handle.net/10675.2/75
Title:
Effect of neutrophil depletion on gelatinase expression, edema formation and hemorrhagic transformation after focal ischemic stroke.
Authors:
Harris, Alex K; Ergul, Adviye; Kozak, Anna; Machado, Livia S; Johnson, Maribeth H.; Fagan, Susan C.
Abstract:
BACKGROUND: While gelatinase (MMP-2 and -9) activity is increased after focal ischemia/reperfusion injury in the brain, the relative contribution of neutrophils to the MMP activity and to the development of hemorrhagic transformation remains unknown. RESULTS: Anti-PMN treatment caused successful depletion of neutrophils in treated animals. There was no difference in either infarct volume or hemorrhage between control and PMN depleted animals. While there were significant increases in gelatinase (MMP-2 and MMP-9) expression and activity and edema formation associated with ischemia, neutrophil depletion failed to cause any change. CONCLUSION: The main finding of this study is that, in the absence of circulating neutrophils, MMP-2 and MMP-9 expression and activity are still up-regulated following focal cerebral ischemia. Additionally, neutrophil depletion had no influence on indicators of ischemic brain damage including edema, hemorrhage, and infarct size. These findings indicate that, at least acutely, neutrophils are not a significant contributor of gelatinase activity associated with acute neurovascular damage after stroke.
Citation:
BMC Neurosci. 2005 Aug 3; 6:49
Issue Date:
25-Aug-2005
URI:
http://hdl.handle.net/10675.2/75
DOI:
10.1186/1471-2202-6-49
PubMed ID:
16078993
PubMed Central ID:
PMC1190186
Type:
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
ISSN:
1471-2202
Appears in Collections:
Vascular Biology Center: Faculty Research and Publication

Full metadata record

DC FieldValue Language
dc.contributor.authorHarris, Alex Ken_US
dc.contributor.authorErgul, Adviyeen_US
dc.contributor.authorKozak, Annaen_US
dc.contributor.authorMachado, Livia Sen_US
dc.contributor.authorJohnson, Maribeth H.en_US
dc.contributor.authorFagan, Susan C.en_US
dc.date.accessioned2010-09-24T21:44:43Z-
dc.date.available2010-09-24T21:44:43Z-
dc.date.issued2005-08-25en_US
dc.identifier.citationBMC Neurosci. 2005 Aug 3; 6:49en_US
dc.identifier.issn1471-2202en_US
dc.identifier.pmid16078993en_US
dc.identifier.doi10.1186/1471-2202-6-49en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/75-
dc.description.abstractBACKGROUND: While gelatinase (MMP-2 and -9) activity is increased after focal ischemia/reperfusion injury in the brain, the relative contribution of neutrophils to the MMP activity and to the development of hemorrhagic transformation remains unknown. RESULTS: Anti-PMN treatment caused successful depletion of neutrophils in treated animals. There was no difference in either infarct volume or hemorrhage between control and PMN depleted animals. While there were significant increases in gelatinase (MMP-2 and MMP-9) expression and activity and edema formation associated with ischemia, neutrophil depletion failed to cause any change. CONCLUSION: The main finding of this study is that, in the absence of circulating neutrophils, MMP-2 and MMP-9 expression and activity are still up-regulated following focal cerebral ischemia. Additionally, neutrophil depletion had no influence on indicators of ischemic brain damage including edema, hemorrhage, and infarct size. These findings indicate that, at least acutely, neutrophils are not a significant contributor of gelatinase activity associated with acute neurovascular damage after stroke.en_US
dc.rightsThe PMC Open Access Subset is a relatively small part of the total collection of articles in PMC. Articles in the PMC Open Access Subset are still protected by copyright, but are made available under a Creative Commons or similar license that generally allows more liberal redistribution and reuse than a traditional copyrighted work. Please refer to the license statement in each article for specific terms of use. The license terms are not identical for all articles in this subset.en_US
dc.subject.meshAnimalsen_US
dc.subject.meshBrain Edema / enzymology / genetics / pathologyen_US
dc.subject.meshBrain Ischemia / enzymology / genetics / pathologyen_US
dc.subject.meshCell Count / methodsen_US
dc.subject.meshGelatinases / biosynthesis / geneticsen_US
dc.subject.meshGene Expression Regulation, Enzymologic / physiologyen_US
dc.subject.meshIntracranial Hemorrhages / enzymology / genetics / pathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshNeutropenia / complications / enzymologyen_US
dc.subject.meshNeutrophils / cytology / enzymologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshStroke / enzymology / genetics / pathologyen_US
dc.titleEffect of neutrophil depletion on gelatinase expression, edema formation and hemorrhagic transformation after focal ischemic stroke.en_US
dc.typeComparative Studyen_US
dc.typeJournal Articleen_US
dc.typeResearch Support, N.I.H., Extramuralen_US
dc.typeResearch Support, Non-U.S. Gov'ten_US
dc.typeResearch Support, U.S. Gov't, P.H.S.en_US
dc.identifier.pmcidPMC1190186en_US
dc.contributor.corporatenameVascular Biology Centeren_US
dc.contributor.corporatenameDepartment of Biostatistics and Epidemiologyen_US
dc.contributor.corporatenameDepartment of Neurologyen_US

Related articles on PubMed

All Items in Scholarly Commons are protected by copyright, with all rights reserved, unless otherwise indicated.