scholarly journals Hyperbaric oxygen preconditioning ameliorates blood-brain barrier damage induced by hypoxia through modulation of tight junction proteins in an in vitro model

2016 ◽  
Vol 57 (1) ◽  
pp. 51-57 ◽  
Author(s):  
Lei Hao ◽  
Xiuming Guo ◽  
Can Zou ◽  
Huchuan Zhou ◽  
Hong Tian ◽  
...  
Keyword(s):  
Tight Junction ◽  
Blood Brain Barrier ◽  
Hyperbaric Oxygen ◽  
In Vitro Model ◽  
Tight Junction Proteins ◽  
Vitro Model ◽  
Hyperbaric Oxygen Preconditioning ◽  
Blood Brain Barrier Damage ◽  
Junction Proteins

Macrophages and dendritic cells express tight junction proteins and exchange particles in an in vitro model of the human airway wall

Immunobiology ◽  
2011 ◽  
Vol 216 (1-2) ◽  
pp. 86-95 ◽  
Author(s):  
Fabian Blank ◽  
Marc Wehrli ◽  
Andrea Lehmann ◽  
Oliver Baum ◽  
Peter Gehr ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Tight Junction ◽  
In Vitro Model ◽  
Tight Junction Proteins ◽  
Airway Wall ◽  
Human Airway ◽  
Vitro Model ◽  
Junction Proteins

scholarly journals MicroRNA-30a regulates acute cerebral ischemia-induced blood–brain barrier damage through ZnT4/zinc pathway

2020 ◽  
pp. 0271678X2092678 ◽  
Author(s):  
Peng Wang ◽  
Rong Pan ◽  
John Weaver ◽  
Mengjie Jia ◽  
Xue Yang ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Tight Junction ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Tight Junction Proteins ◽  
Blood Brain ◽  
Acute Cerebral Ischemia ◽  
Junction Proteins

The mechanism of early blood–brain barrier (BBB) disruption after stroke has been intensively studied but still not fully understood. Here, we report that microRNA-30a (miR-30a) could mediate BBB damage using both cellular and animal models of ischemic stroke. In the experiments in vitro, inhibition of miR-30a decreased BBB permeability, prevented the degradation of tight junction proteins, and reduced intracellular free zinc in endothelial cells. We found that the zinc transporter ZnT4 was a direct target of negative regulation by miR-30a, and ZnT4/zinc signaling pathway contributed significantly to miR-30a-mediated BBB damage. Consistent with these in vitro findings, treatment with miR-30a inhibitor reduced zinc accumulation, increased the expression of ZnT4, and prevented the loss of tight junction proteins in microvessels of ischemic animals. Furthermore, inhibition of miR-30a, even at 90 min post onset of middle cerebral artery occlusion, prevented BBB damage, reduced infarct volume, and ameliorated neurological deficits. Together, our findings provide novel insights into the mechanisms of cerebral ischemia-induced BBB disruption and indicate miR-30a as a regulator of BBB function that can be an effective therapeutic target for ischemic stroke.

PFAS & Pesticides effect on cell Survival, Permeability and Tight Junction in an in-vitro model of the Human Blood-Brain Barrier

2021 ◽  
Vol 350 ◽  
pp. S91
Author(s):  
D. Deepika ◽  
M. Capodiferro ◽  
R. Esplugas ◽  
J. Blanco ◽  
R.P. Sharma ◽  
...  
Keyword(s):  
Tight Junction ◽  
Cell Survival ◽  
Blood Brain Barrier ◽  
Human Blood ◽  
In Vitro Model ◽  
Brain Barrier ◽  
Blood Brain ◽  
Vitro Model

scholarly journals Preeclampsia and Increased Permeability Over the Blood–Brain Barrier: A Role of Vascular Endothelial Growth Receptor 2

2020 ◽  
Author(s):  
Lina Bergman ◽  
Jesenia Acurio ◽  
Jose Leon ◽  
Emily Gatu ◽  
Therese Friis ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tight Junction ◽  
Blood Brain Barrier ◽  
In Vitro Model ◽  
Plasma Concentrations ◽  
Vascular Endothelial ◽  
Vitro Model ◽  
Angiogenic Biomarkers

Abstract BACKGROUND Cerebral complications in preeclampsia are leading causes of maternal mortality worldwide but pathophysiology is largely unknown and a challenge to study. Using an in vitro model of the human blood–brain barrier (BBB), we explored the role of vascular endothelial growth factor receptor 2 (VEGFR2) in preeclampsia. METHODS The human brain endothelial cell line (hCMEC/D3) cultured on Tranwells insert was exposed (12 hours) to plasma from women with preeclampsia (n = 28), normal pregnancy (n = 28), and nonpregnant (n = 16) controls. Transendothelial electrical resistance (TEER) and permeability to 70 kDa fluorescein isothiocyanate (FITC)-dextran were measured for the assessment of BBB integrity. We explored possible underlying mechanisms, with a focus on the expression of tight junction proteins and phosphorylation of 2 tyrosine residues of VEGFR2, associated with vascular permeability and migration (pY951) and cell proliferation (pY1175). Plasma concentrations of soluble FMS-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF) were also measured. RESULTS hCMEC/D3 exposed to plasma from women with preeclampsia exhibited reduced TEER and increased permeability to 70 kDa FITC-dextran. These cells upregulated the messenger ribonucleic acid (mRNA) levels of VEGFR2, and pY951-VEGFR2, but reduced pY1175-VEGFR2 (P < 0.05 in all cases). No difference in mRNA expression of tight junction protein was observed between groups. There was no correlation between angiogenic biomarkers and BBB permeability. CONCLUSIONS We present a promising in vitro model of the BBB in preeclampsia. Selective tyrosine phosphorylation of VEGFR2 may participate in the increased BBB permeability in preeclampsia irrespective of plasma concentrations of angiogenic biomarkers.

scholarly journals The blood-brain barrier studied in vitro across species

PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0236770
Author(s):  
Maj Schneider Thomsen ◽  
Nanna Humle ◽  
Eva Hede ◽  
Torben Moos ◽  
Annette Burkhart ◽  
...  
Keyword(s):  
Tight Junction ◽  
Cell Size ◽  
Blood Brain Barrier ◽  
Transferrin Receptor ◽  
Brain Barrier ◽  
Tight Junction Proteins ◽  
Apparent Permeability ◽  
Blood Brain ◽  
Junction Proteins

The blood-brain barrier (BBB) is formed by brain capillary endothelial cells (BECs) supported by pericytes and astrocytes. The BBB maintains homeostasis and protects the brain against toxic substances circulating in the blood, meaning that only a few drugs can pass the BBB. Thus, for drug screening, understanding cell interactions, and pathology, in vitro BBB models have been developed using BECs from various animal sources. When comparing models of different species, differences exist especially in regards to the transendothelial electrical resistance (TEER). Thus, we compared primary mice, rat, and porcine BECs (mBECs, rBECs, and pBECs) cultured in mono- and co-culture with astrocytes, to identify species-dependent differences that could explain the variations in TEER and aid to the selection of models for future BBB studies. The BBB models based on primary mBECs, rBECs, and pBECs were evaluated and compared in regards to major BBB characteristics. The barrier integrity was evaluated by the expression of tight junction proteins and measurements of TEER and apparent permeability (Papp). Additionally, the cell size, the functionality of the P-glycoprotein (P-gp) efflux transporter, and the expression of the transferrin receptor were evaluated and compared. Expression and organization of tight junction proteins were in all three species influenced by co-culturing, supporting the findings, that TEER increases after co-culturing with astrocytes. All models had functional polarised P-gp efflux transporters and expressed the transferrin receptor. The most interesting discovery was that even though the pBECs had higher TEER than rBECs and mBECs, the Papp did not show the same variation between species, which could be explained by a significantly larger cell size of pBECs. In conclusion, our results imply that the choice of species for a given BBB study should be defined from its purpose, instead of aiming to reach the highest TEER, as the models studied here revealed similar BBB properties.

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