scholarly journals Pretreatment Blood–Brain Barrier Damage and Post-Treatment Intracranial Hemorrhage in Patients Receiving Intravenous Tissue-Type Plasminogen Activator

Stroke ◽  
2014 ◽  
Vol 45 (7) ◽  
pp. 2030-2035 ◽  
Author(s):  
Richard Leigh ◽  
Shyian S. Jen ◽  
Argye E. Hillis ◽  
John W. Krakauer ◽  
Peter B. Barker ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Blood Brain Barrier ◽  
Intracranial Hemorrhage ◽  
Post Treatment ◽  
Brain Barrier ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Blood Brain ◽  
Type Plasminogen Activator ◽  
Blood Brain Barrier Damage

scholarly journals Tissue-type plasminogen activator induces opening of the blood-brain barrier via the LDL receptor–related protein

2003 ◽  
Vol 112 (10) ◽  
pp. 1533-1540 ◽  
Author(s):  
Manuel Yepes ◽  
Maria Sandkvist ◽  
Elizabeth G. Moore ◽  
Thomas H. Bugge ◽  
Dudley K. Strickland ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Blood Brain Barrier ◽  
Ldl Receptor ◽  
Brain Barrier ◽  
Tissue Type ◽  
Related Protein ◽  
Tissue Type Plasminogen Activator ◽  
Blood Brain ◽  
Type Plasminogen Activator

scholarly journals Plasmin-Dependent Modulation of the Blood–Brain Barrier: A Major Consideration during tPA-Induced Thrombolysis?

2014 ◽  
Vol 34 (8) ◽  
pp. 1283-1296 ◽  
Author(s):  
Be'eri Niego ◽  
Robert L Medcalf
Keyword(s):  
Ischemic Stroke ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Tissue Type ◽  
Ischemic Event ◽  
Tissue Type Plasminogen Activator ◽  
Rational Case ◽  
Blood Brain ◽  
Type Plasminogen Activator ◽  
Major Consideration

Plasmin, the principal downstream product of tissue-type plasminogen activator (tPA), is known for its potent fibrin-degrading capacity but is also recognized for many non-fibrinolytic activities. Curiously, plasmin has not been conclusively linked to blood–brain barrier (BBB) disruption during recombinant tPA (rtPA)-induced thrombolysis in ischemic stroke. This is surprising given the substantial involvement of tPA in the modulation of BBB permeability and the co-existence of tPA and plasminogen in both blood and brain throughout the ischemic event. Here, we review the work that argues a role for plasmin together with endogenous tPA or rtPA in BBB alteration, presenting the overall controversy around the topic yet creating a rational case for an involvement of plasmin in this process.

Tissue-type plasminogen activator induces TNF-α-mediated preconditioning of the blood-brain barrier

2021 ◽  
pp. 0271678X2110603
Author(s):  
Ariel Diaz ◽  
Yena Woo ◽  
Cynthia Martin-Jimenez ◽  
Paola Merino ◽  
Enrique Torre ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Blood Brain Barrier ◽  
Neuronal Survival ◽  
Ischemic Tolerance ◽  
Brain Barrier ◽  
Tissue Type ◽  
Ischemic Insult ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Tnf Α

Ischemic tolerance is a phenomenon whereby transient exposure to a non-injurious preconditioning stimulus triggers resistance to a subsequent lethal ischemic insult. Despite the fact that not only neurons but also astrocytes and endothelial cells have a unique response to preconditioning stimuli, current research has been focused mostly on the effect of preconditioning on neuronal death. Thus, it is unclear if the blood-brain barrier (BBB) can be preconditioned independently of an effect on neuronal survival. The release of tissue-type plasminogen activator (tPA) from perivascular astrocytes in response to an ischemic insult increases the permeability of the BBB. In line with these observations, treatment with recombinant tPA increases the permeability of the BBB and genetic deficiency of tPA attenuates the development of post-ischemic edema. Here we show that tPA induces ischemic tolerance in the BBB independently of an effect on neuronal survival. We found that tPA renders the BBB resistant to an ischemic injury by inducing TNF-α-mediated astrocytic activation and increasing the abundance of aquaporin-4-immunoreactive astrocytic end-feet processes in the neurovascular unit. This is a new role for tPA, that does not require plasmin generation, and with potential therapeutic implications for patients with cerebrovascular disease.

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