All Phenotypes Fn1<tm1Ref> MGI Mouse

increased neuron apoptosis ( J:67961 )

• in response to transient focal cerebral ischemia, homozygotes exhibit a significantly increased number of apoptotic neuronal and non-neuronal cells in infarcted areas

• however, no significant differences are observed in cell proliferation, monocyte/macrophage infiltration, neovascularization or initial gliosis

increased susceptibility to ischemic brain injury ( J:67961 )

• homozygotes display increased susceptibility to ischemia/reperfusion cerebral injury relative to wild-type mice, despite a normal brain vasculature

increased cerebral infarct size ( J:67961 )

• in response to transient focal cerebral ischemia, 2-3-mo-old homozygotes exhibit a 35% increase in brain infarct size relative to wild-type mice

homeostasis/metabolism phenotype ( J:67961 )

N

• homozygotes are viable, fertile and anatomically normal with no spontaneous bleeding, normal skin-wound healing, and normal hemostatic parameters, as shown by normal bleeding times and activated partial thromboplastin times, and in vitro plasma clotting activity, platelet aggregation and clot retraction

decreased susceptibility to induced thrombosis ( J:82373 )

• in response to FeCl₃-induced arterial injury, mutants exhibit a delay of several minutes in platelet thrombus formation, despite normal initial platelet vessel wall adhesion

• resulting arterial thrombi are well anchored to the vessel wall but grow slowly with continuous shedding of platelets or small platelet clumps

• platelet/platelet cohesion is reduced and occlusion of injured arterioles is significantly delayed, with most vessels remaining patent at the end of a 40-min observation period