Lost Polarization of Aquaporin4 and Dystroglycan in the Core Lesion after Traumatic Brain Injury Suggests Functional Divergence in Evolution

Hui Liu,Fei Zhuo,Shan Quan Sun,Wei Hua Yu,Mei Yang,Fen Hong Li,Gou Ping Qiu

doi:10.1155/2015/471631

Hui Liu, Fei Zhuo + Show 5 more

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https://doi.org/10.1155/2015/471631

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Abstract

Objective. To understand how aquaporin4 (AQP4) and dystroglycan (DG) polarized distribution change and their roles in brain edema formation after traumatic brain injury (TBI). Methods. Brain water content, Evans blue detection, real-time PCR, western blot, and immunofluorescence were used. Results. At an early stage of TBI, AQP4 and DG maintained vessel-like pattern in perivascular endfeet; M1, M23, and M1/M23 were increased in the core lesion. At a later stage of TBI, DG expression was lost in perivascular area, accompanied with similar but delayed change of AQP4 expression; expression of M1, M23, and DG and the ratio of M1/M2 were increased. Conclusion. At an early stage, AQP4 and DG maintained the polarized distribution. Upregulated M1 and M23 could retard the cytotoxic edema formation. At a later stage AQP4 and DG polarized expression were lost from perivascular endfeet and induced the worst cytotoxic brain edema. The alteration of DG expression could regulate that of AQP4 expression after TBI.

Highlights

ObjectiveTo understand how aquaporin (AQP4) and dystroglycan (DG) polarized distribution change and their roles in brain edema formation after traumatic brain injury (TBI)
Brain edema is a common consequence of traumatic brain injury (TBI)
Cytotoxic edema is caused by energy failure and subsequent accumulation of fluid in the cell resulting in cell swelling, while vasogenic edema occurs when the blood-brain barrier (BBB) becomes leaky permitting influx of plasma constituents into the brain extracellular space [1]

Summary

Objective

To understand how aquaporin (AQP4) and dystroglycan (DG) polarized distribution change and their roles in brain edema formation after traumatic brain injury (TBI). At an early stage of TBI, AQP4 and DG maintained vessel-like pattern in perivascular endfeet; M1, M23, and M1/M23 were increased in the core lesion. At a later stage of TBI, DG expression was lost in perivascular area, accompanied with similar but delayed change of AQP4 expression; expression of M1, M23, and DG and the ratio of M1/M2 were increased. AQP4 and DG maintained the polarized distribution. Upregulated M1 and M23 could retard the cytotoxic edema formation. At a later stage AQP4 and DG polarized expression were lost from perivascular endfeet and induced the worst cytotoxic brain edema. The alteration of DG expression could regulate that of AQP4 expression after TBI

Introduction

Animal and Methods

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Discussion