2016Surgical Neurology InternationalOpen access

The time course changes in expression of aquaporin 4 and aquaporin 1 following global cerebral ischemic edema in rat

Gökhan Akdemir, Figen Kaymaz, Yasemin Özdemir, Nejat Akalan, EkinSu Akdemir

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Abstract

BACKGROUND: The aim of this global cerebral ischemia study was to study the changes in expression levels of aquaporin 4 (AQP4) and AQP1 over time. METHODS: Sprague-Dawley type male rats were divided into six groups. Sham group and ischemia/reperfusion were performed on five other groups using the four-vessel occlusion model. Reperfusion was done 30 min after the occlusion, and each group was tested at 1, 6, 12, 24, and 48 h for brain wet-dry weight ratio and AQP4 and AQP1 expression levels using immunohistochemistry. To prove ischemia development exists in both hippocampal neurons and epithelia of choroid plexus, hematoxylin, and eosin and neuronal marker (NeuN) immune-staining have been applied to the sham experimental group at 48 h. AQP4 expression levels are also measured with western blotting. RESULTS: After ischemia/reperfusion it is observed that the decrease in brain water content between 12 and 24 h was statistically significant (P < 0.01). In parallel and based on immunohistochemical staining, AQP4 expression levels did not exhibit any statistically significant change. AQP4 levels did not show any statistically significant change in western blotting. AQP1 expression in choroid plexus epithelial cells decreased at the 12 and 24 h but increased in 48 h (P < 0.05). CONCLUSIONS: Lack of change in AQP4 expression levels is thought as its dual role in formation and elimination of ischemic brain edema. Decrease in AQP1 expression levels in 24 h can be explained with necrosis in choroid plexus after ischemia and the increase in 48 h mark can be related to recovery in choroid plexus.

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BACKGROUND: The aim of this global cerebral ischemia study was to study the changes in expression levels of aquaporin 4 (AQP4) and AQP1 over time. METHODS: Sprague-Dawley type male rats were divided into six groups. Sham group and ischemia/reperfusion were performed on five other groups using the four-vessel occlusion model. Reperfusion was done 30 min after the occlusion, and each group was tested at 1, 6, 12, 24, and 48 h for brain wet-dry weight ratio and AQP4 and AQP1 expression levels using immunohistochemistry. To prove ischemia development exists in both hippocampal neurons and epithelia of choroid plexus, hematoxylin, and eosin and neuronal marker (NeuN) immune-staining have been applied to the sham experimental group at 48 h. AQP4 expression levels are also measured with western blotting. RESULTS: After ischemia/reperfusion it is observed that the decrease in brain water content between 12 and 24 h was statistically significant (P < 0.01). In parallel and based on immunohistochemical staining, AQP4 expression levels did not exhibit any statistically significant change. AQP4 levels did not show any statistically significant change in western blotting. AQP1 expression in choroid plexus epithelial cells decreased at the 12 and 24 h but increased in 48 h (P < 0.05). CONCLUSIONS: Lack of change in AQP4 expression levels is thought as its dual role in formation and elimination of ischemic brain edema. Decrease in AQP1 expression levels in 24 h can be explained with necrosis in choroid plexus after ischemia and the increase in 48 h mark can be related to recovery in choroid plexus.

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Available abstract

BACKGROUND: The aim of this global cerebral ischemia study was to study the changes in expression levels of aquaporin 4 (AQP4) and AQP1 over time. METHODS: Sprague-Dawley type male rats were divided into six groups. Sham group and ischemia/reperfusion were performed on five other groups using the four-vessel occlusion model. Reperfusion was done 30 min after the occlusion, and each group was tested at 1, 6, 12, 24, and 48 h for brain wet-dry weight ratio and AQP4 and AQP1 expression levels using immunohistochemistry. To prove ischemia development exists in both hippocampal neurons and epithelia of choroid plexus, hematoxylin, and eosin and neuronal marker (NeuN) immune-staining have been applied to the sham experimental group at 48 h. AQP4 expression levels are also measured with western blotting. RESULTS: After ischemia/reperfusion it is observed that the decrease in brain water content between 12 and 24 h was statistically significant (P < 0.01). In parallel and based on immunohistochemical staining, AQP4 expression levels did not exhibit any statistically significant change. AQP4 levels did not show any statistically significant change in western blotting. AQP1 expression in choroid plexus epithelial cells decreased at the 12 and 24 h but increased in 48 h (P < 0.05). CONCLUSIONS: Lack of change in AQP4 expression levels is thought as its dual role in formation and elimination of ischemic brain edema. Decrease in AQP1 expression levels in 24 h can be explained with necrosis in choroid plexus after ischemia and the increase in 48 h mark can be related to recovery in choroid plexus.

Key concepts: Aquaporin 4, Aquaporin 1, Choroid plexus, Ischemia, Medicine, Immunohistochemistry, H&E stain, Hippocampal formation

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