scholarly journals Foxo1‐induced miR‐92b down‐regulation promotes blood‐brain barrier damage after ischaemic stroke by targeting NOX4

2021 ◽  
Author(s):  
Jian Shen ◽  
Ganglei Li ◽  
Yu Zhu ◽  
Qingsheng Xu ◽  
Hengjun Zhou ◽  
...  
Keyword(s):  
Ischaemic Stroke ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Down Regulation ◽  
Blood Brain ◽  
Blood Brain Barrier Damage

scholarly journals PET-MRI nanoparticles imaging of blood–brain barrier damage and modulation after stroke reperfusion

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Justine Debatisse ◽  
Omer Faruk Eker ◽  
Océane Wateau ◽  
Tae-Hee Cho ◽  
Marlène Wiart ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Ischaemic Stroke ◽  
Blood Brain Barrier ◽  
Acute Ischaemic Stroke ◽  
Brain Parenchyma ◽  
Brain Barrier ◽  
Resonance Imaging ◽  
Blood Brain ◽  
Blood Brain Barrier Damage

Abstract In an acute ischaemic stroke, understanding the dynamics of blood–brain barrier injury is of particular importance for the prevention of symptomatic haemorrhagic transformation. However, the available techniques assessing blood–brain barrier permeability are not quantitative and are little used in the context of acute reperfusion therapy. Nanoparticles cross the healthy or impaired blood–brain barrier through combined passive and active processes. Imaging and quantifying their transfer rate could better characterize blood–brain barrier damage and refine the delivery of neuroprotective agents. We previously developed an original endovascular stroke model of acute ischaemic stroke treated by mechanical thrombectomy followed by positron emission tomography-magnetic resonance imaging. Cerebral capillary permeability was quantified for two molecule sizes: small clinical gadolinium Gd-DOTA (<1 nm) and AGuIX® nanoparticles (∼5 nm) used for brain theranostics. On dynamic contrast-enhanced magnetic resonance imaging, the baseline transfer constant Ktrans was 0.94 [0.48, 1.72] and 0.16 [0.08, 0.33] ×10−3 min−1, respectively, in the normal brain parenchyma, consistent with their respective sizes, and 1.90 [1.23, 3.95] and 2.86 [1.39, 4.52] ×10−3 min−1 in choroid plexus, confirming higher permeability than brain parenchyma. At early reperfusion, Ktrans for both Gd-DOTA and AGuIX® nanoparticles was significantly higher within the ischaemic area compared to the contralateral hemisphere; 2.23 [1.17, 4.13] and 0.82 [0.46, 1.87] ×10−3 min−1 for Gd-DOTA and AGuIX® nanoparticles, respectively. With AGuIX® nanoparticles, Ktrans also increased within the ischaemic growth areas, suggesting added value for AGuIX®. Finally, Ktrans was significantly lower in both the lesion and the choroid plexus in a drug-treated group (ciclosporin A, n = 7) compared to placebo (n = 5). Ktrans quantification with AGuIX® nanoparticles can monitor early blood–brain barrier damage and treatment effect in ischaemic stroke after reperfusion.

Angiopoietin-like protein 1 decreases blood brain barrier damage and edema following focal cerebral ischemia in mice

2008 ◽  
Vol 52 (3) ◽  
pp. 470-477 ◽  
Author(s):  
Dar-Ming Lai ◽  
Hung Li ◽  
Chin-Cheng Lee ◽  
Yi-Shiuan Tzeng ◽  
Yu-Hsuan Hsieh ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Blood Brain Barrier ◽  
Focal Cerebral Ischemia ◽  
Brain Barrier ◽  
Blood Brain ◽  
Blood Brain Barrier Damage

Potential of immunoglobuline treatment in motor neuron diseases associated to blood-brain barrier damage

2021 ◽  
Vol 429 ◽  
pp. 119406
Author(s):  
Lucrezia Becattini ◽  
Francesca Bianchi ◽  
Alessandra Govoni ◽  
Erika Schirinzi ◽  
Andrea Bacci ◽  
...  
Keyword(s):  
Motor Neuron ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Motor Neuron Diseases ◽  
Blood Brain ◽  
Blood Brain Barrier Damage

scholarly journals Kininogen deficiency protects from ischemic neurodegeneration in mice by reducing thrombosis, blood-brain barrier damage, and inflammation

Blood ◽  
2012 ◽  
Vol 120 (19) ◽  
pp. 4082-4092 ◽  
Author(s):  
Friederike Langhauser ◽  
Eva Göb ◽  
Peter Kraft ◽  
Christian Geis ◽  
Joachim Schmitt ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Blood Brain Barrier ◽  
Thrombus Formation ◽  
Therapeutic Interventions ◽  
Brain Barrier ◽  
Edema Formation ◽  
Kinin System ◽  
Local Inflammatory Response ◽  
Blood Brain ◽  
Blood Brain Barrier Damage

Abstract Thrombosis and inflammation are hallmarks of ischemic stroke still unamenable to therapeutic interventions. High-molecular-weight kininogen (KNG) is a central constituent of the contact-kinin system which represents an interface between thrombotic and inflammatory circuits and is critically involved in stroke development. Kng−/− mice are protected from thrombosis after artificial vessel wall injury and lack the proinflammatory mediator bradykinin. We investigated the consequences of KNG deficiency in models of ischemic stroke. Kng−/− mice of either sex subjected to transient middle cerebral artery occlusion developed dramatically smaller brain infarctions and less severe neurologic deficits without an increase in infarct-associated hemorrhage. This protective effect was preserved at later stages of infarction as well as in elderly mice. Targeting KNG reduced thrombus formation in ischemic vessels and improved cerebral blood flow, and reconstitution of KNG-deficient mice with human KNG or bradykinin restored clot deposition and infarct susceptibility. Moreover, mice deficient in KNG showed less severe blood-brain barrier damage and edema formation, and the local inflammatory response was reduced compared with controls. Because KNG appears to be instrumental in pathologic thrombus formation and inflammation but dispensable for hemostasis, KNG inhibition may offer a selective and safe strategy for combating stroke and other thromboembolic diseases.

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