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Platelet adhesion receptors do not modulate infarct volume after a photochemically induced stroke in mice
Journal article   Peer reviewed

Platelet adhesion receptors do not modulate infarct volume after a photochemically induced stroke in mice

Kim Frederix, Anil K Chauhan, Janka Kisucka, Bing-Qiao Zhao, Erik I Hoff, Henri M.H Spronk, Hugo ten Cate and Denisa D Wagner
Brain research, Vol.1185(1), pp.239-245
2007
DOI: 10.1016/j.brainres.2007.07.103
PMCID: PMC2692282
PMID: 17996853
url
https://orbi.uliege.be/handle/2268/23143View
Open Access

Abstract

Photochemically induced cerebral infarction has been considered a clinically relevant model for ischemic stroke. We evaluated various transgenic mice to study the role of platelet adhesion molecules in this model. Infarction to the sensorimotoric cortex was induced by erythrosin B and laser light. Infarct volumes were calculated from triphenyltetrazolium chloride stained brain slices. Thrombus formation and vessel leakage were observed in vivo by multiphoton microscopy. Mice mutant in VWF, GPIbα, β3 integrin, and P-selectin did not show any significant differences in infarct volume compared to wild type (WT). This is in contrast to the intraluminal middle cerebral artery occlusion model in which αIIbβ3 integrin, GPIbα, and P-selectin are known to modulate infarct size. Multiphoton microscopy showed that small, non-occlusive embolizing platelet thrombi formed in the photochemically injured brains. Massive vessel leakage was observed within 25 min of laser injury. Interestingly, we observed a significant increase in infarct size with aging, accordant with heightened fragility of the blood brain barrier (BBB) in older mice. This model of photochemically induced stroke is closer to a BBB injury model than a thrombotic stroke model in which platelets and their adhesion molecules are crucial. This model will be useful to study mechanisms regulating BBB permeability.
Aging Photochemically induced stroke Platelet adhesion receptor Blood brain barrier permeability

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