Plasmin-dependent modulation of the blood-brain barrier: a major consideration during tPA-induced thrombolysis?

Research output: Contribution to journalReview ArticleResearchpeer-review

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
Original languageEnglish
Pages (from-to)1283 - 1296
Number of pages14
JournalJournal of Cerebral Blood Flow and Metabolism
Volume34
Issue number8
DOIs
Publication statusPublished - 2014

Cite this

@article{3ef8ead3c3e04c1c957db70b55e167d2,
title = "Plasmin-dependent modulation of the blood-brain barrier: a major consideration during tPA-induced thrombolysis?",
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",
author = "Be'eri Niego and Medcalf, {Robert Lindsay}",
year = "2014",
doi = "10.1038/jcbfm.2014.99",
language = "English",
volume = "34",
pages = "1283 -- 1296",
journal = "Journal of Cerebral Blood Flow and Metabolism",
issn = "0271-678X",
publisher = "Nature Publishing Group",
number = "8",

}

Plasmin-dependent modulation of the blood-brain barrier: a major consideration during tPA-induced thrombolysis? / Niego, Be'eri; Medcalf, Robert Lindsay.

In: Journal of Cerebral Blood Flow and Metabolism, Vol. 34, No. 8, 2014, p. 1283 - 1296.

Research output: Contribution to journalReview ArticleResearchpeer-review

TY - JOUR

T1 - Plasmin-dependent modulation of the blood-brain barrier: a major consideration during tPA-induced thrombolysis?

AU - Niego, Be'eri

AU - Medcalf, Robert Lindsay

PY - 2014

Y1 - 2014

N2 - 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

AB - 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

UR - http://www.nature.com/jcbfm/journal/v34/n8/full/jcbfm201499a.html

U2 - 10.1038/jcbfm.2014.99

DO - 10.1038/jcbfm.2014.99

M3 - Review Article

VL - 34

SP - 1283

EP - 1296

JO - Journal of Cerebral Blood Flow and Metabolism

JF - Journal of Cerebral Blood Flow and Metabolism

SN - 0271-678X

IS - 8

ER -