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Effect of Neutrophil Depletion on Gelatinase Expression, Edema Formation and Hemorrhagic Transformation After Focal Ischemic Stroke

Overview
Journal BMC Neurosci
Publisher Biomed Central
Specialty Neurology
Date 2005 Aug 5
PMID 16078993
Citations 42
Authors
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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.

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References
1.
Ergul A, Portik-Dobos V, Giulumian A, Molero M, Fuchs L . Stress upregulates arterial matrix metalloproteinase expression and activity via endothelin A receptor activation. Am J Physiol Heart Circ Physiol. 2003; 285(5):H2225-32. DOI: 10.1152/ajpheart.00133.2003. View

2.
Fagan S, Nagaraja T, Fenstermacher J, Zheng J, Johnson M, Knight R . Hemorrhagic transformation is related to the duration of occlusion and treatment with tissue plasminogen activator in a nonembolic stroke model. Neurol Res. 2003; 25(4):377-82. DOI: 10.1179/016164103101201526. View

3.
Hilali H, Simpkins A, Hill W, Waller J, Knight R, Fagan S . Single slice method for quantification of hemorrhagic transformation using direct ELISA. Neurol Res. 2004; 26(1):93-8. DOI: 10.1179/016164104773026606. View

4.
Fagan S, Hess D, Hohnadel E, Pollock D, Ergul A . Targets for vascular protection after acute ischemic stroke. Stroke. 2004; 35(9):2220-5. DOI: 10.1161/01.STR.0000138023.60272.9e. View

5.
Maier C, Hsieh L, Yu F, Bracci P, Chan P . Matrix metalloproteinase-9 and myeloperoxidase expression: quantitative analysis by antigen immunohistochemistry in a model of transient focal cerebral ischemia. Stroke. 2004; 35(5):1169-74. DOI: 10.1161/01.STR.0000125861.55804.f2. View