Extended Data Fig. 8: Assessment of neurological deficits and infarct size 1 and 3 days after stroke in Foxf2iECKO and Ctrl mice treated with either vehicle or AKB-9778 prior to fMCAO. | Nature Neuroscience

Extended Data Fig. 8: Assessment of neurological deficits and infarct size 1 and 3 days after stroke in Foxf2iECKO and Ctrl mice treated with either vehicle or AKB-9778 prior to fMCAO.

From: The stroke risk gene Foxf2 maintains brain endothelial cell function via Tie2 signaling

Extended Data Fig. 8: Assessment of neurological deficits and infarct size 1 and 3 days after stroke in Foxf2iECKO and Ctrl mice treated with either vehicle or AKB-9778 prior to fMCAO.

a, Experimental outline. Vehicle or AKB-9778-treated Foxf2iECKO and Ctrl mice underwent middle cerebral artery occlusion (MCAO) followed by Neuroscore analysis and micro-MRI prior to brain dissection and confocal imaging. Neurological deficits and infarct size were determined 1 and 3 days after experimental stroke induction (1 and 3 days post-stroke, dps, respectively). Morphological profiling was performed 3 dps. Panel a was created with BioRender.com. b,c, Quantification of general and focal neurological deficit (b), and infarct size (c) 1 and 3 dps. d, Exemplary magnetic resonance scans from Ctrl-Veh, Foxf2iECKO-Veh, and Foxf2iECKO-AKB mice 1 and 3 dps. Shown are consecutive slices (T2-weighted sequence), scale bar = 5 mm. b,c, Data are presented as mean ± s.d.; comparison by two-tailed unpaired t-test, **p < 0.01; *p < 0.05; b, n = 5 mice per group, c. n = 4 mice per group.

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