Improved long-term outcome after transient cerebral ischemia in aquaporin-4 knockout mice.

ABSTRACT: A hallmark of stroke is water accumulation (edema) resulting from dysregulation of osmotic homeostasis. Brain edema contributes to tissue demise and may lead to increased intracranial pressure and lethal herniation. Currently, there are only limited treatments to prevent edema formation following stroke. Aquaporin 4 (AQP4), a brain water channel, has become a focus of interest for therapeutic approaches targeting edema. At present, there are no pharmacological tools to block AQP4. The role of AQP4 in edema after brain injury remains unclear with conflicting results from studies using AQP4^-/- mice and of AQP4 expression following stroke. Here, we studied AQP4 and its role in edema formation by testing AQP4^-/- mice in a model of middle cerebral artery occlusion using no

SUBMITTER: Hirt L 

PROVIDER: S-EPMC5363745 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature