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dc.contributor.authorHarris, Alex K
dc.contributor.authorErgul, Adviye
dc.contributor.authorKozak, Anna
dc.contributor.authorMachado, Livia S
dc.contributor.authorJohnson, Maribeth H
dc.contributor.authorFagan, Susan C
dc.date.accessioned2013-06-12T15:25:34Z
dc.date.available2013-06-12T15:25:34Z
dc.date.issued2005-08-03
dc.identifier.citationBMC Neuroscience. 2005 Aug 03;6(1):49
dc.identifier.urihttp://dx.doi.org/10.1186/1471-2202-6-49
dc.identifier.urihttp://hdl.handle.net/10724/19807
dc.description.abstractAbstract 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.
dc.titleEffect of neutrophil depletion on gelatinase expression, edema formation and hemorrhagic transformation after focal ischemic stroke
dc.typeJournal Article
dc.date.updated2013-06-07T19:51:44Z
dc.description.versionPeer Reviewed
dc.language.rfc3066en
dc.rights.holderAlex K Harris et al.; licensee BioMed Central Ltd.


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