Blood-Brain Barrier Dysfunction after Primary Blast Injury in vitro

2013 ◽  
Vol 30 (19) ◽  
pp. 1652-1663 ◽  
Author(s):  
Christopher D. Hue ◽  
Siqi Cao ◽  
Syed F. Haider ◽  
Kiet V. Vo ◽  
Gwen B. Effgen ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Blast Injury ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Primary Blast ◽  
Blood Brain

Repeated Primary Blast Injury Causes Delayed Recovery, but not Additive Disruption, in an In Vitro Blood–Brain Barrier Model

2014 ◽  
Vol 31 (10) ◽  
pp. 951-960 ◽  
Author(s):  
Christopher D. Hue ◽  
Siqi Cao ◽  
Cameron R. “Dale” Bass ◽  
David F. Meaney ◽  
Barclay Morrison
Keyword(s):  
Blood Brain Barrier ◽  
Blast Injury ◽  
Brain Barrier ◽  
Primary Blast ◽  
Blood Brain ◽  
Blood Brain Barrier Model ◽  
Delayed Recovery ◽  
Injury Causes ◽  
Barrier Model

scholarly journals Dexamethasone Potentiates in Vitro Blood-Brain Barrier Recovery after Primary Blast Injury by Glucocorticoid Receptor-Mediated Upregulation of ZO-1 Tight Junction Protein

2015 ◽  
Vol 35 (7) ◽  
pp. 1191-1198 ◽  
Author(s):  
Christopher D Hue ◽  
Frances S Cho ◽  
Siqi Cao ◽  
Cameron R “Dale” Bass ◽  
David F Meaney ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Tight Junction ◽  
Blood Brain Barrier ◽  
Blast Injury ◽  
Brain Barrier ◽  
Primary Blast ◽  
Blood Brain ◽  
Junction Protein ◽  
In Vitro Bbb Model

Owing to the frequent incidence of blast-induced traumatic brain injury (bTBI) in recent military conflicts, there is an urgent need to develop effective therapies for bTBI-related pathologies. Blood-brain barrier (BBB) breakdown has been reported to occur after primary blast exposure, making restoration of BBB function and integrity a promising therapeutic target. We tested the hypothesis that treatment with dexamethasone (DEX) after primary blast injury potentiates recovery of an in vitro BBB model consisting of mouse brain endothelial cells (bEnd.3). DEX treatment resulted in complete recovery of transendothelial electrical resistance and hydraulic conductivity 1 day after injury, compared with 3 days for vehicle-treated injured cultures. Administration of RU486 (mifepristone) inhibited effects of DEX, confirming that barrier restoration was mediated by glucocorticoid receptor signaling. Potentiated recovery with DEX treatment was accompanied by stronger zonula occludens (ZO)-1 tight junction immunostaining and expression, suggesting that increased ZO-1 expression was a structural correlate to BBB recovery after blast. Interestingly, augmented ZO-1 protein expression was associated with specific upregulation of the α+ isoform but not the α− isoform. This is the first study to provide a mechanistic basis for potentiated functional recovery of an in vitro BBB model because of glucocorticoid treatment after primary blast injury.

Role of thrombin-PAR1-PKCθ/δ axis in brain pericytes in thrombin-induced MMP-9 production and blood–brain barrier dysfunction in vitro

Neuroscience ◽  
2017 ◽  
Vol 350 ◽  
pp. 146-157 ◽  
Author(s):  
Takashi Machida ◽  
Shinya Dohgu ◽  
Fuyuko Takata ◽  
Junichi Matsumoto ◽  
Ikuya Kimura ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain ◽  
Brain Pericytes

scholarly journals In vitro analysis of drugs that improve hyperglycemia-induced blood-brain barrier dysfunction

2018 ◽  
Vol 503 (3) ◽  
pp. 1885-1890 ◽  
Author(s):  
Ryoma Kayano ◽  
Yoichi Morofuji ◽  
Shinsuke Nakagawa ◽  
Shuji Fukuda ◽  
Daisuke Watanabe ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain ◽  
Vitro Analysis ◽  
In Vitro Analysis

scholarly journals Blood–Brain Barrier Dysfunction in a 3D In Vitro Model of Alzheimer's Disease

2019 ◽  
Vol 6 (20) ◽  
pp. 1900962 ◽  
Author(s):  
Yoojin Shin ◽  
Se Hoon Choi ◽  
Eunhee Kim ◽  
Enjana Bylykbashi ◽  
Jeong Ah Kim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Blood Brain Barrier ◽  
In Vitro Model ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain ◽  
Model Of Alzheimer’S Disease ◽  
3D In Vitro Model ◽  
Vitro Model

Oncostatin-M-Reactive Pericytes Aggravate Blood–Brain Barrier Dysfunction by Activating JAK/STAT3 Signaling In Vitro

Neuroscience ◽  
2019 ◽  
Vol 422 ◽  
pp. 12-20
Author(s):  
Fuyuko Takata ◽  
Shinya Dohgu ◽  
Shinya Sakaguchi ◽  
Kenta Sakai ◽  
Gaku Yamanaka ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Oncostatin M ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Stat3 Signaling ◽  
Blood Brain

scholarly journals Myeloperoxidase-Derived Oxidants Induce Blood-Brain Barrier Dysfunction In Vitro and In Vivo

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e64034 ◽  
Author(s):  
Andreas Üllen ◽  
Evelin Singewald ◽  
Viktoria Konya ◽  
Günter Fauler ◽  
Helga Reicher ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain

scholarly journals Pitavastatin Ameliorates Lipopolysaccharide-Induced Blood-Brain Barrier Dysfunction

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 837
Author(s):  
Takashi Fujimoto ◽  
Yoichi Morofuji ◽  
Andrej Kovac ◽  
Michelle A. Erickson ◽  
Mária A. Deli ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Neurological Diseases ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Neuroprotective Effects ◽  
Blood Brain ◽  
Mouse Brain Endothelial Cells ◽  
Pharmacological Significance ◽  
Primary Mouse

Statins have neuroprotective effects on neurological diseases, including a pleiotropic effect possibly related to blood–brain barrier (BBB) function. In this study, we investigated the effects of pitavastatin (PTV) on lipopolysaccharide (LPS)-induced BBB dysfunction in an in vitro BBB model comprising cocultured primary mouse brain endothelial cells, pericytes, and astrocytes. LPS (1 ng/mL, 24 h) increased the permeability and lowered the transendothelial electrical resistance of the BBB, and the co-administration of PTV prevented these effects. LPS increased the release of interleukin-6, granulocyte colony-stimulating factor, keratinocyte-derived chemokine, monocyte chemotactic protein-1, and regulated on activation, normal T-cell expressed and secreted from the BBB model. PTV inhibited the LPS-induced release of these cytokines. These results suggest that PTV can ameliorate LPS-induced BBB dysfunction, and these effects might be mediated through the inhibition of LPS-induced cytokine production. Clinically, therapeutic approaches using statins combined with novel strategies need to be designed. Our present finding sheds light on the pharmacological significance of statins in the treatment of central nervous system diseases.

Ιmmunity, Vascular Aging, and Stroke

2022 ◽  
Vol 29 ◽  
Author(s):  
Anna-Maria Louka ◽  
Dimitrios Sagris ◽  
George Ntaios
Keyword(s):  
Blood Brain Barrier ◽  
Molecular Mechanisms ◽  
Vascular Dysfunction ◽  
Vascular Inflammation ◽  
Brain Barrier ◽  
Low Grade ◽  
Vascular Aging ◽  
Barrier Dysfunction ◽  
Blood Brain

Abstract: Stroke is one of the most devastating manifestations of cardiovascular disease. Growing age, arterial hypertension, and atherosclerosis are identified as independent risk factors for stroke, primarily due to structural and functional alterations in the cerebrovascular tree. Recent data from in vitro and clinical studies have suggested that the immune system influences atherosclerosis, promoting vascular stiffness and vascular aging and contributing to ischemic stroke, intracranial haemorrhage and microbleeds, white matter disease, and cognitive decline. Furthermore, aging is related to a chronic low-grade inflammatory state, in which macrophage, neutrophils, natural killer (NK cells), and B and T lymphocytes act as major effectors of the immune-mediated cell responses. Moreover, oxidative stress and vascular inflammation are correlated with endothelial dysfunction, vascular aging, blood-brain barrier disruption, lacunar lesions, and neurodegenerative disorders. This review discusses the pathophysiological roles of fundamental cellular and molecular mechanisms of aging, including the complex interplay between them and innate immunity, as well as vascular dysfunction, arterial stiffness, atherosclerosis, atherothrombosis, systemic inflammation, and blood-brain barrier dysfunction.

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