Reactive Oxygen Species-Caspase-3 Relationship in Mediating Blood-Brain Barrier Endothelial Cell Hyperpermeability Following Oxygen-Glucose Deprivation and Reoxygenation

2014 ◽  
Vol 21 (2) ◽  
pp. 187-195 ◽  
Author(s):  
Himakarnika Alluri ◽  
Hayden W. Stagg ◽  
Rickesha L. Wilson ◽  
Robert P. Clayton ◽  
Devendra A. Sawant ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cell ◽  
Blood Brain Barrier ◽  
Caspase 3 ◽  
Reactive Oxygen ◽  
Glucose Deprivation ◽  
Brain Barrier ◽  
Oxygen Glucose Deprivation ◽  
Oxygen Species ◽  
Blood Brain

scholarly journals DDIS-17. POLYNITROXYL ALBUMIN INHIBITS BRAIN TUMORIGENIC CASCADE THROUGH A REACTIVE OXYGEN SPECIES MECHANISM ACROSS THE BLOOD BRAIN BARRIER

2017 ◽  
Vol 19 (suppl_6) ◽  
pp. vi62-vi62
Author(s):  
Katie Grausam ◽  
Ross Lanier ◽  
Amanda Schaefer ◽  
Li Ma ◽  
Bohdan Soltys ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Blood Brain Barrier ◽  
Reactive Oxygen ◽  
Brain Barrier ◽  
Oxygen Species ◽  
Blood Brain

scholarly journals Mitochondrial Mechanisms That Regulate Blood‐Brain Barrier Endothelial Cell Hyperpermeability Following Oxygen‐Glucose Deprivation and Reoxygenation

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Himakarnika Alluri ◽  
Robert Patrick Clayton ◽  
Devendra Sawant ◽  
Hayden W Stagg ◽  
Rickesha L Wilson ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Blood Brain Barrier ◽  
Glucose Deprivation ◽  
Brain Barrier ◽  
Oxygen Glucose Deprivation ◽  
Blood Brain

Reactive oxygen species enhance the migration of monocytes across the blood‐brain barrier in vitro

2001 ◽  
Vol 15 (10) ◽  
pp. 1852-1854 ◽  
Author(s):  
Annette Goes ◽  
Diana Wouters ◽  
Susanne M. A. Pol ◽  
Ruth Huizinga ◽  
Eric Ronken ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Blood Brain Barrier ◽  
Reactive Oxygen ◽  
Brain Barrier ◽  
Oxygen Species ◽  
Blood Brain

scholarly journals Alcohol-Induced Blood-Brain Barrier Impairment: An In Vitro Study

2021 ◽  
Vol 18 (5) ◽  
pp. 2683
Author(s):  
Donatello Carrino ◽  
Jacopo Junio Valerio Branca ◽  
Matteo Becatti ◽  
Ferdinando Paternostro ◽  
Gabriele Morucci ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Tight Junction ◽  
Blood Brain Barrier ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Brain Barrier ◽  
Oxygen Species ◽  
Blood Brain ◽  
Species Production

In recent years, alcohol abuse has dramatically grown with deleterious consequence for people’s health and, in turn, for health care costs. It has been demonstrated, in humans and animals, that alcohol intoxication induces neuroinflammation and neurodegeneration thus leading to brain impairments. Furthermore, it has been shown that alcohol consumption is able to impair the blood–brain barrier (BBB), but the molecular mechanisms underlining this detrimental effect have not been fully elucidated. For this reason, in this study we investigated the effects of alcohol exposure on a rat brain endothelial (RBE4) cell line, as an in vitro-validated model of brain microvascular endothelial cells. To assess whether alcohol caused a concentration-related response, the cells were treated at different times with increasing concentrations (10–1713 mM) of ethyl alcohol (EtOH). Microscopic and molecular techniques, such as cell viability assay, immunofluorescence and Western blotting, were used to examine the mechanisms involved in alcohol-induced brain endothelial cell alterations including tight junction distribution, apoptosis, and reactive oxygen species production. Our findings clearly demonstrate that alcohol causes the formation of gaps between cells by tight junction disassembly, triggered by the endoplasmic reticulum and oxidative stress, highlighted by GRP78 chaperone upregulation and increase in reactive oxygen species production, respectively. The results from this study shed light on the mechanisms underlying alcohol-induced blood–brain barrier dysfunction and a better understanding of these processes will allow us to take advantage of developing new therapeutic strategies in order to prevent the deleterious effects of alcohol.

Exacerbation of oxygen–glucose deprivation-induced blood–brain barrier disruption: potential pathogenic role of interleukin-9 in ischemic stroke

2017 ◽  
Vol 131 (13) ◽  
pp. 1499-1513 ◽  
Author(s):  
Sha Tan ◽  
Yilong Shan ◽  
Yuge Wang ◽  
Yinyao Lin ◽  
Siyuan Liao ◽  
...  
Keyword(s):  
T Cells ◽  
Ischemic Stroke ◽  
Blood Brain Barrier ◽  
Mononuclear Cells ◽  
Biological Effects ◽  
Glucose Deprivation ◽  
Brain Barrier ◽  
Oxygen Glucose Deprivation ◽  
Expression Levels ◽  
Blood Brain

Interleukin (IL)-9 exerts a variety of functions in autoimmune diseases. However, its role in ischemic brain injury remains unknown. The present study explored the biological effects of IL-9 in ischemic stroke (IS). We recruited 42 patients newly diagnosed with IS and 22 age- and sex-matched healthy controls. The expression levels of IL-9 and percentages of IL-9-producing T cells, including CD3+CD4+IL-9+ and CD3+CD8+IL-9+ cells, were determined in peripheral blood mononuclear cells (PBMCs) obtained from patients and control individuals. We also investigated the effects of IL-9 on the blood–brain barrier (BBB) following oxygen–glucose deprivation (OGD) and the potential downstream signaling pathways. We found that patients with IS had higher IL-9 expression levels and increased percentages of IL-9-producing T cells in their PBMCs. The percentages of CD3+CD4+IL-9+ and CD3+CD8+IL-9+ T cells were positively correlated with the severity of illness. In in vitro experiments using bEnd.3 cells, exogenously administered IL-9 exacerbated the loss of tight junction proteins (TJPs) in cells subjected to OGD plus reoxygenation (RO). This effect was mediated via activation of IL-9 receptors, which increased the level of endothelial nitric oxide synthase (eNOS), as well as through up-regulated phosphorylation of signal transducer and activator of transcription 1 and 3 and down-regulated phosphorylated protein kinase B/phosphorylated phosphatidylinositol 3-kinase signaling. These results indicate that IL-9 has a destructive effect on the BBB following OGD, at least in part by inducing eNOS production, and raise the possibility of targetting IL-9 for therapeutic intervention in IS.

scholarly journals Mice deficient in endothelial α5 integrin are profoundly resistant to experimental ischemic stroke

2016 ◽  
Vol 37 (1) ◽  
pp. 85-96 ◽  
Author(s):  
Jill Roberts ◽  
Leon de Hoog ◽  
Gregory J Bix
Keyword(s):  
Endothelial Cell ◽  
Blood Brain Barrier ◽  
Infarct Volume ◽  
Ischemic Injury ◽  
Glucose Deprivation ◽  
Brain Barrier ◽  
Barrier Integrity ◽  
Blood Brain ◽  
Blood Brain Barrier Integrity

Stroke is a disease in dire need of better therapies. We have previously shown that a fragment of the extracellular matrix proteoglycan, perlecan, has beneficial effects following cerebral ischemia via the α5β1 integrin receptor. We now report that endothelial cell selective α5 integrin deficient mice (α5 KO) are profoundly resistant to ischemic infarct after transient middle cerebral artery occlusion. Specifically, α5 KOs had little to no infarct 2–3 days post-stroke, whereas controls had an increase in mean infarct volume over the same time period as expected. Functional outcome is also improved in the α5 KOs compared with controls. Importantly, no differences in cerebrovascular anatomy or collateral blood flow were noted that could account for this difference in ischemic injury. Rather, we demonstrate that α5 KOs have increased blood-brain barrier integrity (increased expression of claudin-5, and absent brain parenchymal IgG extravasation) after stroke compared with controls, which could explain their resistance to ischemic injury. Additionally, inhibition of α5 integrin in vitro leads to decreased permeability of brain endothelial cells following oxygen-glucose deprivation. Together, these findings indicate endothelial cell α5 integrin plays an important role in stroke outcome and blood-brain barrier integrity, suggesting that α5 integrin could be a novel therapeutic target for stroke.

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