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Status epilepticus induces vasogenic edema via tumor necrosis factor-α/ endothelin-1-mediated two different pathways

PloS one, 2013-09, Vol.8 (9), p.e74458-e74458 [Peer Reviewed Journal]

2013 Kim et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2013 Kim et al 2013 Kim et al ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0074458 ;PMID: 24040253

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Title:
Status epilepticus induces vasogenic edema via tumor necrosis factor-α/ endothelin-1-mediated two different pathways
Author: Kim, Ji-Eun ; Ryu, Hea Jin ; Kang, Tae-Cheon
Mongin, Alexander A.
Subjects: Activation ; Animals ; Astrocytes ; Astrocytes - metabolism ; Astrocytes - pathology ; Blood-brain barrier ; Blood-Brain Barrier - metabolism ; Blood-Brain Barrier - pathology ; Brain Edema - etiology ; Brain Edema - genetics ; Brain Edema - metabolism ; Brain Edema - pathology ; Brain research ; Cerebral Cortex - metabolism ; Cerebral Cortex - pathology ; Cortex (piriform) ; Disease Models, Animal ; Edema ; Endothelial cells ; Endothelial Cells - metabolism ; Endothelial Cells - pathology ; Endothelin 1 ; Endothelin-1 - genetics ; Endothelin-1 - metabolism ; Epilepsy ; Gene Expression Regulation ; Laboratories ; Male ; Medicine ; Membrane permeability ; Microdialysis ; Mortality ; NAD(P)H oxidase ; NADPH Oxidases - genetics ; NADPH Oxidases - metabolism ; Neurobiology ; Neurological diseases ; Neurons - metabolism ; Neurons - pathology ; Neurosciences ; Nitric oxide ; Nitric Oxide Synthase Type III - genetics ; Nitric Oxide Synthase Type III - metabolism ; Nitric-oxide synthase ; Oxidase ; Oxygen ; Permeability ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Receptor mechanisms ; Receptor, Endothelin A - genetics ; Receptor, Endothelin A - metabolism ; Rodents ; Signal Transduction ; Status Epilepticus - complications ; Status Epilepticus - genetics ; Status Epilepticus - metabolism ; Status Epilepticus - pathology ; Stereotaxic Techniques ; Stroke ; Surgery ; TNF inhibitors ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α
Is Part Of: PloS one, 2013-09, Vol.8 (9), p.e74458-e74458
Description: Status epilepticus (SE) induces vasogenic edema in the piriform cortex with disruptions of the blood-brain barrier (BBB). However, the mechanisms of vasogenic edema formation following SE are still unknown. Here we investigated the endothelin B (ETB) receptor-mediated pathway of SE-induced vasogenic edema. Following SE, the release of tumor necrosis factor-α (TNF-α) stimulated endothelin-1 (ET-1) release and expression in neurons and endothelial cells. In addition, TNF-α-induced ET-1 increased BBB permeability via ETB receptor-mediated endothelial nitric oxide synthase (eNOS) activation in endothelial cells. ETB receptor activation also increased intracellular reactive oxygen species by NADPH oxidase production in astrocytes. These findings suggest that SE results in BBB dysfunctions via endothelial-astroglial interactions through the TNF-α-ET-1-eNOS/NADPH oxidase pathway, and that these ETB receptor-mediated interactions may be an effective therapeutic strategy for vasogenic edema in various neurological diseases.
Publisher: United States: Public Library of Science
Language: English
Identifier: ISSN: 1932-6203
EISSN: 1932-6203
DOI: 10.1371/journal.pone.0074458
PMID: 24040253
Source: GFMER Free Medical Journals
MEDLINE
PubMed Central
Public Library of Science (PLoS)
ProQuest Central
DOAJ Directory of Open Access Journals

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Status epilepticus induces vasogenic edema via tumor necrosis factor-α/ endothelin-1-mediated two different pathways

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