Oxygen–glucose deprivation increases the enzymatic activity and the microvesicle-mediated release of ectonucleotidases in the cells composing the blood–brain barrier

2011 ◽  
Vol 59 (2) ◽  
pp. 259-271 ◽  
Author(s):  
Stefania Ceruti ◽  
Laura Colombo ◽  
Giulia Magni ◽  
Francesca Viganò ◽  
Marta Boccazzi ◽  
...  
Keyword(s):  
Enzymatic Activity ◽  
Blood Brain Barrier ◽  
Glucose Deprivation ◽  
Brain Barrier ◽  
Oxygen Glucose Deprivation ◽  
Blood Brain

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 Oxygen Glucose Deprivation Switches the Transport of tPA Across the Blood–Brain Barrier From an LRP-Dependent to an Increased LRP-Independent Process

Stroke ◽  
2005 ◽  
Vol 36 (5) ◽  
pp. 1059-1064 ◽  
Author(s):  
Karim Benchenane ◽  
Vincent Berezowski ◽  
Mónica Fernández-Monreal ◽  
Julien Brillault ◽  
Samuel Valable ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Glucose Deprivation ◽  
Brain Barrier ◽  
Oxygen Glucose Deprivation ◽  
Blood Brain ◽  
Independent Process

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

scholarly journals A Functional Role for Sodium-Dependent Glucose Transport across the Blood-Brain Barrier during Oxygen Glucose Deprivation

2008 ◽  
Vol 328 (2) ◽  
pp. 487-495 ◽  
Author(s):  
Sharanya Vemula ◽  
Karen E. Roder ◽  
Tianzhi Yang ◽  
G. Jayarama Bhat ◽  
Thomas J. Thekkumkara ◽  
...  
Keyword(s):  
Glucose Transport ◽  
Blood Brain Barrier ◽  
Functional Role ◽  
Glucose Deprivation ◽  
Brain Barrier ◽  
Oxygen Glucose Deprivation ◽  
Blood Brain ◽  
Sodium Dependent
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