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

Oncostatin M–induced blood‐brain barrier impairment is due to prolonged activation of STAT3 signaling in vitro

2018 ◽  
Vol 119 (11) ◽  
pp. 9055-9063 ◽  
Author(s):  
Fuyuko Takata ◽  
Shinya Dohgu ◽  
Junichi Matsumoto ◽  
Takashi Machida ◽  
Shinya Sakaguchi ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Oncostatin M ◽  
Brain Barrier ◽  
Stat3 Signaling ◽  
Blood Brain

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

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

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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