scholarly journals Procarboxypeptidase U (proCPU, TAFI, proCPB2) in cerebrospinal fluid during ischemic stroke is associated with stroke progression, outcome and blood-brain barrier dysfunction

2017 ◽  
Vol 16 (2) ◽  
pp. 342-348 ◽  
Author(s):  
J. C. Mertens ◽  
D. Leenaerts ◽  
R. Brouns ◽  
S. Engelborghs ◽  
M. Ieven ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Ischemic Stroke ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain

scholarly journals Endothelium-targeted deletion of the miR-15a/16-1 cluster ameliorates blood-brain barrier dysfunction in ischemic stroke

2020 ◽  
Vol 13 (626) ◽  
pp. eaay5686 ◽  
Author(s):  
Feifei Ma ◽  
Ping Sun ◽  
Xuejing Zhang ◽  
Milton H. Hamblin ◽  
Ke-Jie Yin
Keyword(s):  
Ischemic Stroke ◽  
Blood Brain Barrier ◽  
Molecular Mechanisms ◽  
Neuronal Loss ◽  
Glucose Deprivation ◽  
Brain Barrier ◽  
Protein Abundance ◽  
Barrier Dysfunction ◽  
Small Noncoding Rnas ◽  
Blood Brain

The blood-brain barrier (BBB) maintains a stable brain microenvironment. Breakdown of BBB integrity during cerebral ischemia initiates a devastating cascade of events that eventually leads to neuronal loss. MicroRNAs are small noncoding RNAs that suppress protein expression, and we previously showed that the miR-15a/16-1 cluster is involved in the pathogenesis of ischemic brain injury. Here, we demonstrated that when subjected to experimentally induced stroke, mice with an endothelial cell (EC)–selective deletion of miR-15a/16-1 had smaller brain infarcts, reduced BBB leakage, and decreased infiltration of peripheral immune cells. These mice also showed reduced infiltration of proinflammatory M1-type microglia/macrophage in the peri-infarct area without changes in the number of resolving M2-type cells. Stroke decreases claudin-5 abundance, and we found that EC-selective miR-15a/16-1 deletion enhanced claudin-5 mRNA and protein abundance in ischemic mouse brains. In cultured mouse brain microvascular ECs (mBMECs), the miR-15a/16-1 cluster directly bound to the 3′ untranslated region (3′UTR) of Claudin-5, and lentivirus-mediated ablation of miR-15a/16-1 diminished oxygen-glucose deprivation (OGD)–induced down-regulation of claudin-5 mRNA and protein abundance and endothelial barrier dysfunction. These findings suggest that genetic deletion of endothelial miR-15a/16-1 suppresses BBB pathologies after ischemic stroke. Elucidating the molecular mechanisms of miR-15a/16-1–mediated BBB dysfunction may enable the discovery of new therapies for ischemic stroke.

Cerebrospinal fluid and serum nitric oxide metabolites in patients with multiple sclerosis

1998 ◽  
Vol 4 (1) ◽  
pp. 27-30 ◽  
Author(s):  
G Giovannoni
Keyword(s):  
Nitric Oxide ◽  
Multiple Sclerosis ◽  
Cerebrospinal Fluid ◽  
Blood Brain Barrier ◽  
Neurological Diseases ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain ◽  
Nitric Oxide Metabolites ◽  
Nitrate And Nitrite

Nitric oxide is hypothesised to play a role in the immunopathogenesis of multiple sclerosis. Raised cerebrospinal fluid and serum levels of the nitric oxide metabolites nitrate and nitrite have been described in patients with multiple sclerosis. Cerebrospinal fluid and serum nitrate and nitrite were measured in patients with multiple sclerosis, inflammatory and non-inflammatory neurological diseases, and correlated with the albumin quotient, an index of blood-brain-barrier dysfunction. Patients undergoing diagnostic lumbar and vene puncture were prospectively recruited, clinical data were obtained from the hospital records, and the CSF and serum nitrate and nitrite levels were measured by the nitrate reductase and Griess reaction methods. Nitrate and nitrite, were raised in the CSF and serum of patients with multiple sclerosis and other inflammatory neurological diseases compared to patients with non-inflammatory neurological disorders (median nitrate and nitrite: cerebrospinal fluid=10.3 μM vs 15.4 μMvs 6.6 μM, P50.001, and serum=49.0 μM vs 46.4 μM vs 38.8 μM, P=0.02, respectively). CSF nitrate and nitrite levels correlated with the albumin quotient (n=59, r=0.42, P50.001). This study provides further evidence for a role of nitric oxide in the immunopathogenesis of multiple sclerosis and supports a role for nitric oxide as a possible mediator of inflammatory blood-brain-barrier dysfunction.

scholarly journals Blood-brain barrier dysfunction and recovery after ischemic stroke

2018 ◽  
Vol 163-164 ◽  
pp. 144-171 ◽  
Author(s):  
Xiaoyan Jiang ◽  
Anuska V. Andjelkovic ◽  
Ling Zhu ◽  
Tuo Yang ◽  
Michael V.L. Bennett ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain

Attenuated Blood-Brain Barrier Dysfunction by XQ-1H Following Ischemic Stroke in Hyperlipidemic Rats

2014 ◽  
Vol 52 (1) ◽  
pp. 162-175 ◽  
Author(s):  
Weirong Fang ◽  
Lan Sha ◽  
Nandani Darshika Kodithuwakku ◽  
Jie Wei ◽  
Rui Zhang ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain

scholarly journals Soluble CD146, a cerebrospinal fluid marker for neuroinflammation, promotes blood-brain barrier dysfunction

Theranostics ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 231-246 ◽  
Author(s):  
Daji Wang ◽  
Hongxia Duan ◽  
Jing Feng ◽  
Jianquan Xiang ◽  
Liqun Feng ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain ◽  
Soluble Cd146

Cerebrospinal Fluid Markers of Brain Injury, Inflammation, and Blood-Brain Barrier Dysfunction in Cardiac Surgery

2012 ◽  
Vol 94 (2) ◽  
pp. 549-555 ◽  
Author(s):  
Björn Reinsfelt ◽  
Sven-Erik Ricksten ◽  
Henrik Zetterberg ◽  
Kaj Blennow ◽  
Johan Fredén-Lindqvist ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Cardiac Surgery ◽  
Brain Injury ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain
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