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Título

Neutrophil Infiltration Increases Matrix Metalloproteinase-9 in the Ischemic Brain after Occlusion/Reperfusion of the Middle Cerebral Artery in Rats

AutorJusticia, Carles ; Panés, Julián; Solé, Sònia; Cervera, Álvaro; Deulofeu, Ramon; Chamorro, Ángel; Planas, Anna M.
Palabras claveStroke
Neutropenia
MMP-9
Inflammation
ICAM-1
Gelatinase
Fecha de publicacióndic-2003
EditorLippincott Williams & Wilkins
CitaciónJournal of Cerebral Blood Flow and Metabolism 23: 1430-1440 (2003)
ResumenMatrix metalloproteinase-9 (MMP-9) activity increases in the brain during the first day after focal ischemia and might be involved in the pathogenesis of tissue damage. We previously showed MMP-9 in the extracellular space of brain parenchyma along with neutrophil recruitment after ischemia. In the present study, we tested whether neutrophils were a direct source of enhanced MMP-9 in the ischemic brain. Neutrophil infiltration was prevented either by injecting an antibody against ICAM-1, which abrogates neutrophil adhesion to the endothelial vessel wall, or by inducing neutropenia. One-hour intraluminal middle cerebral artery occlusion with reperfusion was induced, and studies were performed at 24 hours. Circulating neutrophils expressed 95-kDa MMP-9 and dimers, and infiltrated neutrophils stained positive for MMP-9. The expression of MMP-9 (mainly 95-kDa proform and dimers and, to a lesser extent, 88-kDa form) increased in brain after ischemia/reperfusion. Treatments preventing neutrophil infiltration failed to preclude the ischemia-induced increase in 88-kDa MMP-9 form and gelatinase activity in neurons and blood vessels. However, these treatments prevented the major increase in 95-kDa MMP-9 form and dimers. We conclude that neutrophil infiltration highly contributes to enhanced MMP-9 in the ischemic brain by releasing MMP-9 proform, which might participate in the tissular inflammatory reaction.
Versión del editorhttp://dx.doi.org/10.1097/01.WCB.0000090680.07515.C8
URIhttp://hdl.handle.net/10261/116806
DOI10.1097/01.WCB.0000090680.07515.C8
Identificadoresdoi: 10.1097/01.WCB.0000090680.07515.C8
issn: 0271-678X
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