Premium
Fibrin‐modifying serine proteases thrombin, tPA, and plasmin in ischemic stroke: A review
Author(s) -
Sheehan John J.,
Tsirka Stella E.
Publication year - 2005
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20150
Subject(s) - plasmin , proteases , tissue plasminogen activator , stroke (engine) , fibrin , thrombin , ischemia , brain ischemia , medicine , thrombus , microglia , blood–brain barrier , cardiology , biology , neuroscience , central nervous system , platelet , immunology , inflammation , biochemistry , enzyme , mechanical engineering , engineering
Ischemic stroke is a sudden loss of circulation to a portion of the brain that results in a loss of neurologic function. Many ischemic strokes are embolic. They result from a thrombus traveling into the central circulation and occluding a blood vessel. Treatment of ischemic stroke with recombinant tissue plasminogen activator (tPA) can improve patient outcomes. However, tPA must be used during a specific time window after the stroke onset to be effective and it risks converting an ischemic stroke into a hemorrhagic one. We explore the basic effects of fibrin‐modifying proteases on neurons, astrocytes, and microglia during ischemia. tPA, thrombin, and plasmin can initiate microglial activation and change both neuronal and astrocytic survival. As a result of these functions and of their role in blood homeostasis, all three of these proteases have profound effects on neurons and glial cells in the brain and are capable of altering the development and severity of ischemic stroke. © 2005 Wiley‐Liss, Inc.