Impact of the neutrophil response to granulocyte colony-stimulating factor on the risk of hemorrhage when used in combination with tissue plasminogen activator during the acute phase of experimental stroke

Granulocyte colony-stimulating factor (G-CSF) is a pharmacologic agent inducing neutrophil mobilization and a new candidate for neuroprotection and neuroregeneration in stroke. Its effects when used in combination with tissue plasminogen activator (tPA) were explored during the acute phase of ischem...

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Published in:Journal of neuroinflammation 2014-05, Vol.11 (1), p.96-96
Main Authors: Gautier, Sophie, Ouk, Thavarak, Tagzirt, Madjid, Lefebvre, Catherine, Laprais, Maud, Pétrault, Olivier, Dupont, Annabelle, Leys, Didier, Bordet, Régis
Format: Article
Language:English
Subjects:
Animals
Brain Infarction - etiology
Disease Models, Animal
Drug Administration Schedule
Endothelium
Endothelium - drug effects
Enzymes
Fibrinolytic Agents - adverse effects
Granulocyte Colony-Stimulating Factor - administration & dosage
Hemorrhage
Hemorrhage - chemically induced
Infarction, Middle Cerebral Artery - drug therapy
Ischemia
Male
Matrix Metalloproteinase 9 - metabolism
Neutrophil Infiltration - drug effects
Neutrophils - drug effects
Neutrophils - metabolism
Peroxidase - metabolism
Rats
Rats, Inbred SHR
Reperfusion Injury - drug therapy
Reperfusion Injury - etiology
Rodents
Statistics, Nonparametric
Surgery
Time Factors
Tissue Plasminogen Activator - adverse effects
Veins & arteries
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cited_by cdi_FETCH-LOGICAL-c591t-29ef713cb164f86d64ab858b947cd5643885730eb342830518b3743f040733453
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container_title Journal of neuroinflammation
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creator Gautier, Sophie
Ouk, Thavarak
Tagzirt, Madjid
Lefebvre, Catherine
Laprais, Maud
Pétrault, Olivier
Dupont, Annabelle
Leys, Didier
Bordet, Régis
description Granulocyte colony-stimulating factor (G-CSF) is a pharmacologic agent inducing neutrophil mobilization and a new candidate for neuroprotection and neuroregeneration in stroke. Its effects when used in combination with tissue plasminogen activator (tPA) were explored during the acute phase of ischemic stroke. We used a middle cerebral artery occlusion (MCAO) model of cerebral ischemia, associated with treatment with tPA, in male spontaneously hypertensive rats (SHR). Granulocyte colony-stimulating factor (G-CSF; 60 μg/kg) was injected just before tPA. Neutrophil response in peripheral blood and in the infarct area was quantified in parallel to the infarct volume. Protease matrix metallopeptidase 9 (MMP-9) release from circulating neutrophils was analyzed by immunochemistry and zymography. Vascular reactivity and hemorrhagic volume in the infarct area was also assessed. Twenty four hours after ischemia and tPA, G-CSF administration induced a significant increase of neutrophils in peripheral blood (P
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Its effects when used in combination with tissue plasminogen activator (tPA) were explored during the acute phase of ischemic stroke. We used a middle cerebral artery occlusion (MCAO) model of cerebral ischemia, associated with treatment with tPA, in male spontaneously hypertensive rats (SHR). Granulocyte colony-stimulating factor (G-CSF; 60 μg/kg) was injected just before tPA. Neutrophil response in peripheral blood and in the infarct area was quantified in parallel to the infarct volume. Protease matrix metallopeptidase 9 (MMP-9) release from circulating neutrophils was analyzed by immunochemistry and zymography. Vascular reactivity and hemorrhagic volume in the infarct area was also assessed. Twenty four hours after ischemia and tPA, G-CSF administration induced a significant increase of neutrophils in peripheral blood (P &lt;0.05). At 72 hours post-ischemia, G-CSF was significantly associated with an increased risk of hemorrhage in the infarct area (2.5 times more likely; P &lt;0.05) and significant cerebral endothelium-dependent dysfunction. Ex vivo, an increased MMP-9 release from neutrophils after tPA administration correlated to the increased hemorrhagic risk (P &lt;0.05). In parallel, G-CSF administration was associated with a decreased neutrophil infiltration in the infarct area (-50%; P &lt;0.05), with a concomitant significant neuroprotective effect (infarct volume: -40%; P &lt;0.05). We demonstrate that G-CSF potentiates the risk of hemorrhage in experimental stroke when used in combination with tPA by inducing neutrophilia. This effect is concomitant to an increased MMP-9 release from peripheral neutrophils induced by the tPA treatment. These results highlight the potential hemorrhagic risk of associating G-CSF to thrombolysis during the acute phase of stroke.</description><identifier>ISSN: 1742-2094</identifier><identifier>EISSN: 1742-2094</identifier><identifier>DOI: 10.1186/1742-2094-11-96</identifier><identifier>PMID: 24885160</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Animals ; Brain Infarction - etiology ; Disease Models, Animal ; Drug Administration Schedule ; Endothelium ; Endothelium - drug effects ; Enzymes ; Fibrinolytic Agents - adverse effects ; Granulocyte Colony-Stimulating Factor - administration &amp; dosage ; Hemorrhage ; Hemorrhage - chemically induced ; Infarction, Middle Cerebral Artery - drug therapy ; Ischemia ; Male ; Matrix Metalloproteinase 9 - metabolism ; Neutrophil Infiltration - drug effects ; Neutrophils - drug effects ; Neutrophils - metabolism ; Peroxidase - metabolism ; Rats ; Rats, Inbred SHR ; Reperfusion Injury - drug therapy ; Reperfusion Injury - etiology ; Rodents ; Statistics, Nonparametric ; Surgery ; Time Factors ; Tissue Plasminogen Activator - adverse effects ; Veins &amp; arteries</subject><ispartof>Journal of neuroinflammation, 2014-05, Vol.11 (1), p.96-96</ispartof><rights>COPYRIGHT 2014 BioMed Central Ltd.</rights><rights>2014 Gautier et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. 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At 72 hours post-ischemia, G-CSF was significantly associated with an increased risk of hemorrhage in the infarct area (2.5 times more likely; P &lt;0.05) and significant cerebral endothelium-dependent dysfunction. Ex vivo, an increased MMP-9 release from neutrophils after tPA administration correlated to the increased hemorrhagic risk (P &lt;0.05). In parallel, G-CSF administration was associated with a decreased neutrophil infiltration in the infarct area (-50%; P &lt;0.05), with a concomitant significant neuroprotective effect (infarct volume: -40%; P &lt;0.05). We demonstrate that G-CSF potentiates the risk of hemorrhage in experimental stroke when used in combination with tPA by inducing neutrophilia. This effect is concomitant to an increased MMP-9 release from peripheral neutrophils induced by the tPA treatment. 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subjects Animals
Brain Infarction - etiology
Disease Models, Animal
Drug Administration Schedule
Endothelium
Endothelium - drug effects
Enzymes
Fibrinolytic Agents - adverse effects
Granulocyte Colony-Stimulating Factor - administration & dosage
Hemorrhage
Hemorrhage - chemically induced
Infarction, Middle Cerebral Artery - drug therapy
Ischemia
Male
Matrix Metalloproteinase 9 - metabolism
Neutrophil Infiltration - drug effects
Neutrophils - drug effects
Neutrophils - metabolism
Peroxidase - metabolism
Rats
Rats, Inbred SHR
Reperfusion Injury - drug therapy
Reperfusion Injury - etiology
Rodents
Statistics, Nonparametric
Surgery
Time Factors
Tissue Plasminogen Activator - adverse effects
Veins & arteries
title Impact of the neutrophil response to granulocyte colony-stimulating factor on the risk of hemorrhage when used in combination with tissue plasminogen activator during the acute phase of experimental stroke
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