scholarly journals Alterations of Blood-Brain Barrier and Associated Factors in Acute Liver Failure

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Wei Cui ◽  
Cui-Ming Sun ◽  
Pei Liu
Keyword(s):  
Tight Junction ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Brain Edema ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Brain Capillary ◽  
Blood Brain ◽  
Capillary Endothelial Cells

Brain edema in acute liver failure (ALF) remains lethal. Cytotoxic mechanisms associated with brain edema have been well recognized, but the role of vasogenic mechanisms of brain edema has not been explored. Intact tight junctions (TJs) between brain capillary endothelial cells are critical for normal BBB function. Recent reports found significant alterations in the tight junction elements including occludin and claudin-5, suggesting a vasogenic injury in the blood-brain barrier (BBB) integrity. However, the role of TJ in ALF has not been completely understood. This paper reviews the role of the paracellular tight junction in the increased selective BBB permeability that leads to brain edema in ALF and furthermore explores the effect of systemic inflammatory cytokines on the tight junction dysfunction.

Receptor-mediated transcytosis of transferrin through blood-brain barrier endothelial cells

1996 ◽  
Vol 270 (4) ◽  
pp. H1149-H1158 ◽  
Author(s):  
L. Descamps ◽  
M. P. Dehouck ◽  
G. Torpier ◽  
R. Cecchelli
Keyword(s):  
Endothelial Cells ◽  
Blood Brain Barrier ◽  
Bovine Brain ◽  
Brain Barrier ◽  
Double Labeling ◽  
Brain Capillary ◽  
Brain Capillary Endothelial Cells ◽  
Blood Brain ◽  
Capillary Endothelial Cells ◽  
A Cell

A cell culture model of the blood-brain barrier consisting of a coculture of bovine brain capillary endothelial cells (BBCECs) and astrocytes has been used to examine the mechanism of iron transport to the brain. Binding experiments showed that BBCECs express 35,000 high-affinity (concn at 50% receptor saturation = 11.3 +/- 2.1 nM) transferin (Tf) receptors per cell. In contrast to apo-transferrin (apoTf) we observed a specific transport of holo-transferrin (holoTf) across BBCECs. This transport was inhibited completely at low temperature. Moreover, the anti-Tf receptor antibody (OX-26) competitively inhibited holoTf uptake by BBCECs. Pulse-chase experiments demonstrated that only 10% of Tf was recycled to the luminal side of the cells, whereas the majority of Tf was transcytosed to the abluminal side; double-labeling experiments clearly demonstrated that iron crosses BBCECs bound to Tf. No intraendothelial degradation of Tf was observed, suggesting that the intraendothelial pathway through BBCECs bypasses the lysosomal compartment. These results clearly show that the iron-Tf complex is transcytosed across brain capillary endothelial cells by a receptor-mediated pathway without any degradation.

scholarly journals Novel Role of MCP-Induced Protein 1 in Ischemic Brain Damage in Animals of Transient Focal Ischemia

2018 ◽  
Author(s):  
Zhuqing Jin ◽  
Jian Liang ◽  
Jiaqi Li ◽  
Pappachan E. Kolattukudy
Keyword(s):  
Cerebral Ischemia ◽  
Matrix Metalloproteinases ◽  
Tight Junction ◽  
Western Blot ◽  
Blood Brain Barrier ◽  
Wild Type Mouse ◽  
Brain Barrier ◽  
Wild Type ◽  
Blood Brain

Focal cerebral ischemia can lead to blood-brain barrier (BBB) breakdown, which is implicated in neuroinflammation and elevation of matrix metalloproteinases (MMPs). The role of the anti-inflammatory protein, monocyte chemotactic protein–induced protein 1 (MCPIP1) plays in the injury of BBB in stroke has not yet been reported. This study was conducted to identify and characterize the role MCPIP1 plays in BBB breakdown. Transient middle cerebral artery occlusion (MCAO) is induced in both wild-type and Mcpip1-/- mice for 2 hours of occlusion periods followed by reperfusion for 24 or 48 hours. BBB permeability was measured by FITC-dextran extravasation, MMP-9/3 expression was analyzed by western blot, and claudin-5 and zonula occludens-1 (ZO-1) were analyzed by immunohistochemistry and western blot. After MCAO in wild type mouse is induced, there is significantly increase in MCPIP1 mRNA and protein levels. Absence of MCPIP1 leaded to significant increase in FITC-dextran leakage in peri-infarct brain, significant upregulation of MMP-9, MMP-3 and reduced levels of tight junction components, claudin-5 and ZO-1 in the brain after MCAO. Our data demonstrate that absence of MCPIP1 exacerbates ischemia-induced blood-brain barrier disruption by enhancing the expression of matrix metalloproteinases and degradation of tight junction proteins. Overall data indicate that MCPIP1 is important protective role against BBB disruption in cerebral ischemia.

scholarly journals Blood-brain barrier damage and brain penetration of antiepileptic drugs: Role of serum proteins and brain edema

Epilepsia ◽  
2009 ◽  
Vol 50 (4) ◽  
pp. 664-677 ◽  
Author(s):  
Nicola Marchi ◽  
Giulia Betto ◽  
Vincent Fazio ◽  
Quinyuan Fan ◽  
Chaitali Ghosh ◽  
...  
Keyword(s):  
Brain Edema ◽  
Antiepileptic Drugs ◽  
Blood Brain Barrier ◽  
Serum Proteins ◽  
Brain Barrier ◽  
Brain Penetration ◽  
Blood Brain ◽  
Blood Brain Barrier Damage

scholarly journals TNAP and EHD1 Are Over-Expressed in Bovine Brain Capillary Endothelial Cells after the Re-Induction of Blood-Brain Barrier Properties

PLoS ONE ◽  
2012 ◽  
Vol 7 (10) ◽  
pp. e48428 ◽  
Author(s):  
Barbara Deracinois ◽  
Sophie Duban-Deweer ◽  
Gwënaël Pottiez ◽  
Roméo Cecchelli ◽  
Yannis Karamanos ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Brain Barrier ◽  
Barrier Properties ◽  
Bovine Brain ◽  
Brain Barrier ◽  
Brain Capillary ◽  
Brain Capillary Endothelial Cells ◽  
Blood Brain ◽  
Capillary Endothelial Cells
Sign in / Sign up

Export Citation Format

Share Document