Glial cells and neurons induce blood-brain barrier related enzymes in cultured cerebral endothelial cells

1991 ◽  
Vol 539 (2) ◽  
pp. 247-253 ◽  
Author(s):  
Ulrike Tontsch ◽  
Hans-Christian Bauer
Keyword(s):  
Endothelial Cells ◽  
Blood Brain Barrier ◽  
Glial Cells ◽  
Brain Barrier ◽  
Cerebral Endothelial Cells ◽  
Blood Brain

scholarly journals Mechanisms of Glutamate Efflux at the Blood—Brain Barrier: Involvement of Glial Cells

2011 ◽  
Vol 32 (1) ◽  
pp. 177-189 ◽  
Author(s):  
Katayun Cohen-Kashi-Malina ◽  
Itzik Cooper ◽  
Vivian I Teichberg
Keyword(s):  
Endothelial Cells ◽  
Blood Brain Barrier ◽  
Glial Cells ◽  
Excitatory Amino Acid ◽  
Active Role ◽  
In Vitro Models ◽  
Brain Barrier ◽  
Amino Acid Transporters ◽  
Blood Brain

At high concentrations, glutamate (Glu) exerts potent neurotoxic properties, leading to irreversible brain damages found in numerous neurological disorders. The accepted notion that Glu homeostasis in brain interstitial fluid is maintained primarily through the activity of Glu transporters present on glial cells does not take into account the possible contribution of endothelial cells constituting the blood-brain barrier (BBB) to this process. Here, we present evidence for the presence of the Glu transporters, excitatory amino-acid transporters (EAATs) 1 to 3, in porcine brain endothelial cells (PBECs) and show their participation in Glu uptake into PBECs. Moreover, transport of Glu across three in vitro models of the BBB is investigated for the first time, and evidence for Glu transport across the BBB in both directions is presented. Our results provide evidence that the BBB can function in the efflux mode to selectively remove Glu, via specific transporters, from the abluminal side (brain) into the luminal compartment (blood). Furthermore, we found that glial cells lining the BBB have an active role in the efflux process by taking up Glu and releasing it, through hemichannels, anion channels, and possibly the reversal of its EAATs, in close proximity to ECs, which in turn take up Glu and release it to the blood.

Induction of blood-brain barrier properties in cultured brain capillary endothelial cells: Comparison between primary glial cells and C6 cell line

Glia ◽  
2005 ◽  
Vol 51 (3) ◽  
pp. 187-198 ◽  
Author(s):  
Monica Boveri ◽  
Vincent Berezowski ◽  
Anna Price ◽  
Stephanie Slupek ◽  
Anne-Marie Lenfant ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Line ◽  
Blood Brain Barrier ◽  
Glial Cells ◽  
Barrier Properties ◽  
Brain Barrier ◽  
Brain Capillary ◽  
Blood Brain ◽  
Capillary Endothelial Cells ◽  
C6 Cell Line

scholarly journals AKAP12 Supports Blood-Brain Barrier Integrity against Ischemic Stroke

2020 ◽  
Vol 21 (23) ◽  
pp. 9078
Author(s):  
Ji Hae Seo ◽  
Takakuni Maki ◽  
Nobukazu Miyamoto ◽  
Yoon Kyong Choi ◽  
Kelly K. Chung ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Brain Barrier ◽  
Knockout Mice ◽  
Kinase Inhibitor ◽  
Rho Kinase ◽  
Endothelial Permeability ◽  
Brain Barrier ◽  
Scaffolding Protein ◽  
Cerebral Endothelial Cells ◽  
Blood Brain

A-kinase anchor protein 12 (AKAP12) is a scaffolding protein that associates with intracellular molecules to regulate multiple signal transductions. Although the roles of AKAP12 in the central nervous system are still relatively understudied, it was previously shown that AKAP12 regulates blood-retinal barrier formation. In this study, we asked whether AKAP12 also supports the function and integrity of the blood-brain barrier (BBB). In a mouse model of focal ischemia, the expression level of AKAP12 in cerebral endothelial cells was upregulated during the acute phase of stroke. Also, in cultured cerebral endothelial cells, oxygen-glucose deprivation induced the upregulation of AKAP12. When AKAP12 expression was suppressed by an siRNA approach in cultured endothelial cells, endothelial permeability was increased along with the dysregulation of ZO-1/Claudin 5 expression. In addition, the loss of AKAP12 expression caused an upregulation/activation of the Rho kinase pathway, and treatment of Rho kinase inhibitor Y-27632 mitigated the increase of endothelial permeability in AKAP12-deficient endothelial cell cultures. These in vitro findings were confirmed by our in vivo experiments using Akap12 knockout mice. Compared to wild-type mice, Akap12 knockout mice showed a larger extent of BBB damage after stroke. However, the inhibition of rho kinase by Y-27632 tightened the BBB in Akap12 knockout mice. These data may suggest that endogenous AKAP12 works to alleviate the damage and dysfunction of the BBB caused by ischemic stress. Therefore, the AKAP12-rho-kinase signaling pathway represents a novel therapeutic target for stroke.

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