Related Experiment Video
Updated: May 7, 2026

Use of a Wireless Video-EEG System to Monitor Epileptiform Discharges Following Lateral Fluid-Percussion Induced Traumatic Brain Injury
Published on: June 21, 2019
Status epilepticus induces vasogenic edema via tumor necrosis factor-α/ endothelin-1-mediated two different pathways
Ji-Eun Kim1, Hea Jin Ryu, Tae-Cheon Kang
1Department of Anatomy and Neurobiology, College of Medicine, Hallym University, Chunchon, Kangwon-Do, Republic of Korea ; Institute of Epilepsy Research, College of Medicine, Hallym University, Chunchon, Kangwon-Do, Republic of Korea.
Abstract:
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.
Related Concept Videos
Cerebral Edema ll: Pathophysiology
Cytotoxic Edema: Pathophysiology
Cerebral Edema l: Introduction
Bacterial Meningitis II: Pathophysiology
Encephalitis ll: Pathophysiology
Ischemic Stroke ll: Pathophysiology

