Mechanisms of Astrocyte-Mediated Cerebral Edema
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- 作者：Jesse A. Stokum (1)
David B. Kurland (1)
Volodymyr Gerzanich (1)
J. Marc Simard (1) (2) (3)
1. Department of Neurosurgery ; University of Maryland School of Medicine ; 22 S. Greene St. ; Suite S12D ; Baltimore ; MD ; 21201-1595 ; USA
2. Department of Pathology ; University of Maryland School of Medicine ; Baltimore ; MD ; 21201-1595 ; USA
3. Department of Physiology ; University of Maryland School of Medicine ; Baltimore ; MD ; 21201-1595 ; USA - 关键词：Cerebral edema ; Blood brain barrier ; Astrocyte ; Aquaporin 4
- 刊名：Neurochemical Research
- 出版年：2015
- 出版时间：February 2015
- 年：2015
- 卷：40
- 期：2
- 页码：317-328
- 全文大小：971 KB
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134. Pasantes-Morales H, Vazquez-Juarez E (2012) Transporters and channels in cytotoxic astrocyte swelling. Neurochem Res 37:2379鈥?387 - 刊物类别：Biomedical and Life Sciences
- 刊物主题：Biomedicine
Neurosciences
Biochemistry
Neurology - 出版者：Springer Netherlands
- ISSN：1573-6903
文摘
Cerebral edema formation stems from disruption of blood brain barrier (BBB) integrity and occurs after injury to the CNS. Due to the restrictive skull, relatively small increases in brain volume can translate into impaired tissue perfusion and brain herniation. In excess, cerebral edema can be gravely harmful. Astrocytes are key participants in cerebral edema by virtue of their relationship with the cerebral vasculature, their unique compliment of solute and water transport proteins, and their general role in brain volume homeostasis. Following the discovery of aquaporins, passive conduits of water flow, aquaporin 4 (AQP4) was identified as the predominant astrocyte water channel. Normally, AQP4 is highly enriched at perivascular endfeet, the outermost layer of the BBB, whereas after injury, AQP4 expression disseminates to the entire astrocytic plasmalemma, a phenomenon termed dysregulation. Arguably, the most important role of AQP4 is to rapidly neutralize osmotic gradients generated by ionic transporters. In pathological conditions, AQP4 is believed to be intimately involved in the formation and clearance of cerebral edema. In this review, we discuss aquaporin function and localization in the BBB during health and injury, and we examine post-injury ionic events that modulate AQP4-dependent edema formation.