• Xiaoming Yao, Nikita Derugin, Geoffrey T Manley, and A S Verkman.
• Department of Neurological Surgery, University of California, San Francisco, CA 94143, USA; Brain and Spinal Injury Center, University of California, San Francisco, CA 94143, USA; Departments of Medicine and Physiology, University of California, San Francisco, CA 94143, USA. Electronic address: xiaoming.yao@ucsf.edu.
• Neurosci. Lett. 2015 Jan 1;584:368-72.

AbstractAquaporin-4 (AQP4) is a water channel expressed in astrocyte end-feet lining the blood-brain barrier. AQP4 deletion in mice is associated with improved outcomes in global cerebral ischemia produced by transient carotid artery occlusion, and focal cerebral ischemia produced by permanent middle cerebral artery occlusion (MCAO). Here, we investigated the consequences of 1-h transient MCAO produced by intraluminal suture blockade followed by 23 h of reperfusion. In nine AQP4(+/+) and nine AQP4(-/-) mice, infarct volume was significantly reduced by an average of 39 ± 4% at 24h in AQP4(-/-) mice, cerebral hemispheric edema was reduced by 23 ± 3%, and Evans Blue extravasation was reduced by 31 ± 2% (mean ± SEM). Diffusion-weighted magnetic resonance imaging showed greatest reduction in apparent diffusion coefficient around the occlusion site after reperfusion, with remarkably lesser reduction in AQP4(-/-) mice. The reduced infarct volume in AQP4(-/-) mice following transient MCAO supports the potential utility of therapeutic AQP4 inhibition in stroke.Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

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