Related Experiment Video
Updated: Apr 28, 2026

Improved Method for the Preparation of a Human Cell-based, Contact Model of the Blood-Brain Barrier
Published on: November 12, 2013
Plasmin-dependent modulation of the blood-brain barrier: a major consideration during tPA-induced thrombolysis?
Be'eri Niego1, Robert L Medcalf1
1Australian Centre for Blood Diseases, Monash University, Melbourne, Victoria, Australia.
Abstract:
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.
Related Concept Videos
The Blood-brain Barrier
Clot Retraction and Fibrinolysis
Cerebral Edema ll: Pathophysiology
Hemorrhagic Stroke ll: Pathophysiology
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Anticoagulant Drugs: Low-Molecular-Weight Heparins

