Thrombin-Activatable Fibrinolysis Inhibitor (TAFI) Deficient Mice Are Susceptible to Intracerebral Thrombosis and Ischemic Stroke
Figure 2
TAFI deficiency does not improve outcome after experimental stroke in mice.
Infarct size and functional outcome in TAFI-/- mice and controls (WT, wild-type) 24h after 60 min transient middle cerebral artery occlusion (tMCAO). (A) (top) Representative 2,3,5-Triphenyltetrazoliumchloride (TTC)-stained coronal brain sections from the two animal groups. Ischemic infarctions appear white and regularly include the neocortex and basal ganglia as confirmed by hematoxylin and eosin (H&E) staining (bar represents 250 µm, dotted white line indicates the border between the cortex and the basal ganglia). (bottom) Infarct volumes on day 1 after tMCAO in TAFI-/- mice and controls as determined by planimetry (n = 11–12/group). Non-parametric Mann Whitney test. (B) Neurological Bederson score and grip test score on day 1 after tMCAO in TAFI-/- mice and controls. In line with the results on infarct volumes, no significant functional differences became apparent. Non-parametric Mann Whitney test (C) Accumulation of fibrin(ogen) in the infarcted (+) and contralateral (−) cortices of TAFI-/- mice and controls. Fibrin(ogen) was analyzed by immunoblotting 24 h after ischemia. Two representative immunoblots of each group are shown.