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2015 ; 40
(2
): 317-28
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Mechanisms of astrocyte-mediated cerebral edema
#MMPMID24996934
Stokum JA
; Kurland DB
; Gerzanich V
; Simard JM
Neurochem Res
2015[Feb]; 40
(2
): 317-28
PMID24996934
show ga
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.
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