%0 Journal Article
%T Platelet glycoprotein Ib¦Á is an important mediator of ischemic stroke in mice
%A Simon F De Meyer
%A Tobias Schwarz
%A Daphne Schatzberg
%A Denisa D Wagner
%J Experimental & Translational Stroke Medicine
%D 2011
%I BioMed Central
%R 10.1186/2040-7378-3-9
%X In this study, we used transgenic mice in which the extracellular part of GPIb¦Á is replaced by human interleukin 4-receptor (GPIb¦Á/IL4R¦Á). We observed normal brain vasculature in these mice. We compared infarct size in GPIb¦Á/IL4R¦Á and wild-type (WT) mice 23 hours after 1-hour transient middle cerebral artery occlusion (tMCAO). In addition, the functional outcome was evaluated using a modified Bederson score.We found a significantly smaller infarct size in GPIb¦Á/IL4R¦Á mice compared to WT mice (38.0 ¡À 6.5 mm3 vs. 74.2 ¡À 8.6 mm3, p < 0.001). The decrease in infarct size was functionally relevant as indicated by a significantly better functional Bederson score in GPIb¦Á/IL4R¦Á mice compared to WT animals (1.3 ¡À 0.4 vs. 2.7 ¡À 0.3, p < 0.05).Our data illustrate and further confirm the important role of platelet GPIb¦Á in ischemic stroke, suggesting that targeted inhibition of this receptor may open new avenues in stroke treatment.Stroke is one of the leading causes of death worldwide with limited treatment options [1]. Platelets play a pivotal role in cerebral ischemia/reperfusion injury by adhering to the damaged vessel wall, leading to further platelet recruitment and thrombus formation. The glycoprotein (GP) Ib-IX-V complex is a crucial platelet receptor for initial tethering and adhesion at sites of vascular injury. This abundant complex on the platelet surface (12,500 copies per cell) consists of the leucine-rich repeat glycoproteins GPIb¦Á, GPIb¦Â, GPIX and GPV in a 2:2:2:1 ratio [2]. The adhesive function of GPIb-IX-V is mainly attributed to the interaction of GPIb¦Á with its major ligand von Willebrand factor (VWF), exposed upon vascular damage. The central role of the GPIb¦Á-VWF interaction in mediating initial platelet adhesion is illustrated by the bleeding disorders Bernard Soulier syndrome [3] and von Willebrand disease [4], caused by deficiency of GPIb-IX-V or VWF respectively. Besides its interaction with VWF, GPIb¦Á can also engage counter-receptors such as ¦ÁM¦Â2 (
%U http://www.etsmjournal.com/content/3/1/9