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. Author manuscript; available in PMC: 2016 Jul 1.
Published in final edited form as: Stroke. 2015 Jun 11;46(7):1956–1965. doi: 10.1161/STROKEAHA.115.008939

Figure 1. Genetic deletion of WNK3 in vivo decreases infarct volume and demyelination and improves neurological recovery following ischemic stroke.

Figure 1

A. Changes in regional cerebral blood flow (rCBF) during and after 60-min MCAO are similar in littermate wild type (WT) and WNK3 KO mice. Values are mean ± SD. *p < 0.05 vs. -15 min, #p < 0.05 vs 0 min with one-way ANOVA . Representative coronal brain sections from WT and WNK3 KO mice. Infarct volume at 24 h Rp was determined by TTC staining. Values are mean ± SEM (n = 8, 4F/4M). *p < 0.05 vs. WT. B. WNK3 KO mice exhibit less white matter injury after MCAO than WT. Left panel: Bright field images of WT (i) or WNK3 KO brain sections (ii) stained with Luxol Fast Blue (LFB) and cresyl violet. Black box: Demyelination analysis in external capsules (EC) of white matter in the CL and IL hemispheres. Right panel: higher magnification images. Arrowhead: myelinated or demyelinated axonal bundles. Arrow: Axonal track. Right panel, Summary of demyelination data. Values are Mean ± SEM (n = 3). *p < 0.05 vs. WT. C. Improved neurological behavior in WNK3 KO mice after MCAO, scored as described in Methods 27. Values are median composite values and data analyzed by non-parametric Mann-Whitney test (n= 8-9, M). *p < 0.05 vs. WT, #p < 0.05 vs. 0 day. D. Expression of pNKCC1 in cytosolic or membrane fractions of ischemic brains. Values are Mean ± SEM (n= 3-4). *p < 0.05 vs. CL.