Increased chromosomal radiosensitivity of a Chinese hamster ovary cell line that inducibly expresses the Eco RI restriction endonuclease

Winegar, Richard A.; Land, Max; Morgan, William F.

doi:10.1016/s0006-291x(89)80113-5

Cited by 2 publications

(1 citation statement)

References 5 publications

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“…The cytokines generated by macrophages and neutrophils can induce activation of JAK-STAT [163], NF-κB [164], and Smad [165,166] signaling pathways leading to an inflammatory response involving cell adhesion, permeability, and apoptosis in ECs [167,168]. Further, these pathways modify the activity of vasodilatory mediators such as NO, PGI2, EDHF, and bradykinin, as well as vasoconstrictive mediators such as ET-1 and angiotensin II ( [169][170][171]). In addition, ROS, TNF-α, and IL-1β produced by activated microglia can disrupt the BBB integrity by altering the expression of ZO-1, claudin-5, occludin, and P-glycoprotein [172].…”

Section: Inflammationmentioning

confidence: 99%

Endothelial Cell Dysfunction and Injury in Subarachnoid Hemorrhage

Kumar¹,

McBride²,

Dash³

et al. 2018

Mol Neurobiol

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In the brain, vascular endothelial cells conserve blood viscosity, control blood flow, and form the interface between central nervous system and circulating blood. Clinical outcome after aneurysmal subarachnoid hemorrhage is linked to early brain injury, cerebral vasospasm, and other causes of delayed cerebral ischemia. The cerebral vasculature remains a unique target for therapies since it becomes rapidly disrupted after subarachnoid hemorrhage, and damage to the blood vessels continues into the delayed injury phase. The current failure of therapies to improve clinical outcome warrants a re-evaluation of current therapeutic approaches. The mechanisms of endothelial cell injury and blood-brain barrier breakdown are critical to the pathway of cerebral injury, and an improved understanding of these mechanisms may lead to novel therapeutic targets. This review provides an update on the current understanding of endothelial cell injury following aneurysmal subarachnoid hemorrhage, including blood-brain barrier dysfunction.

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