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http://hdl.handle.net/1942/13210
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DC Field | Value | Language |
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dc.contributor.author | DE JONGH, Rafael | - |
dc.contributor.author | Nuydens, R. | - |
dc.contributor.author | SMETS, Anke | - |
dc.contributor.author | Vissers, K. | - |
dc.contributor.author | MEERT, Theo | - |
dc.date.accessioned | 2012-02-27T12:31:38Z | - |
dc.date.available | 2012-02-27T12:31:38Z | - |
dc.date.issued | 2008 | - |
dc.identifier.citation | Current Topics in Pharmacology, 12 (2), p. 37-99 | - |
dc.identifier.issn | 0972-4559 | - |
dc.identifier.uri | http://hdl.handle.net/1942/13210 | - |
dc.description.abstract | Water diffusion across lipid bilayers is slow and mainly depends on osmotic forces. In biological membranes, aquaporins (AQPs), facilitate the bi-directional water transport through the lipid bilayer. AQP-4 is the most widely expressed AQP in the brain and is present on astrocyte end-feet surrounding capillaries or lining the pia and ventricles. Neither oligodendrocytes nor neurons express AQP-4, but microglia can be stimulated to synthetize the water channel. There are two isoforms of the AQP-4 protein, called M1 and M23. The expression ratio of these determines the assembly in orthogonal arrays of particles and the functionality of the waterchannels. In vitro, AQP-4 expression can be influenced through the addition of solutes or changes in culture conditions. During pathology, AQP-4 is upregulated in vasogenic brain edema typically found in or around tumors. Cytotoxic edema is encountered during acute hyponatraemia or ischemia/reperfusion and is frequently accompanied by upregulation of AQP-4. This might contribute to early cytotoxic edema formation but also facilitate the clearance of extracellular water during the later phases of edema. After traumatic brain injury, AQP-4 is downregulated in the contusion core, but slightly upregulated in the pericontusional areas. Drug-induced upregulation or reinstitution of perivascular location of AQP-4 after traumatic brain injury by eg., sulphoraphane or magnesium, attenuates post-traumatic brain swelling. During neuromyelitis optica, antibodies against AQP-4 are found in sera and seem to be responsible for eliciting the disease. AQP-4 forms an interesting target for drug discovery to improve the outcome of patients who suffer from brain edema. | - |
dc.language.iso | en | - |
dc.subject.other | aquaporin; brain; water homeostasis; review | - |
dc.title | Aquaporin-4 in the brain: a review | - |
dc.type | Journal Contribution | - |
dc.identifier.epage | 99 | - |
dc.identifier.issue | 2 | - |
dc.identifier.spage | 37 | - |
dc.identifier.volume | 12 | - |
local.bibliographicCitation.jcat | A2 | - |
local.type.refereed | Refereed | - |
local.type.specified | Review | - |
dc.bibliographicCitation.oldjcat | A2 | - |
item.accessRights | Closed Access | - |
item.fulltext | No Fulltext | - |
item.fullcitation | DE JONGH, Rafael; Nuydens, R.; SMETS, Anke; Vissers, K. & MEERT, Theo (2008) Aquaporin-4 in the brain: a review. In: Current Topics in Pharmacology, 12 (2), p. 37-99. | - |
item.contributor | DE JONGH, Rafael | - |
item.contributor | Nuydens, R. | - |
item.contributor | SMETS, Anke | - |
item.contributor | Vissers, K. | - |
item.contributor | MEERT, Theo | - |
crisitem.journal.issn | 0972-4559 | - |
Appears in Collections: | Research publications |
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