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Title: Plasminogen and cell migration in vivo
Authors: Plow, EF
Ploplis, VA
Carmeliet, Peter
Collen, Desire #
Issue Date: Mar-1999
Publisher: Churchill livingstone
Host Document: Fibrinolysis & proteolysis vol:13 issue:2 pages:49-53
Conference: IVth International Congress on Firbrinolysis and Thrombolysis edition:4 location:Ljubljana date:JUN 22-26, 1998
Abstract: In addition to its participation in fibrinolysis, plasminogen is believed to play an important role in mediating cell migration. The development of mice in which the plasminogen gene has been inactivated (Plg(-/-) mice) has provided an opportunity to address the contributions of plasminogen to cell migratory events in an in vivo setting. This article summarizes, some recent studies in which cell migration has been evaluated in the Plg(-/-) mice. In models of inflammation; wound healing, both extravascular and intravascular; atherosclerosis; and tumorogenesis, plasminogen-deficient mice have exhibited altered cell migration compared to wild-type animals. In general, plasminogen deficiency suppresses cell migration, and it is suggested that plasminogen facilitates and, in some circumstances, can be required for a migratory response. By contributing to cell migration, plasminogen can influence a variety of physiologic and pathophysiologic events, in some cases accelerating, and in other cases retarding these responses. This influence of plasminogen may be dependent upon its capacity to degrade fibrin, its capacity to degrade other matrix proteins, its activation of matrix metalloproteinases, or its generation of cytokines, growth factors and other modulators. Taken together, these analyses establish a role of plasminogen and cell migration in vivo and call for further studies to establish the breadth and the molecular mechanisms for this influence.
URI: 
ISSN: 0268-9499
Publication status: published
KU Leuven publication type: IC
Appears in Collections:Vesalius Research Centre (-)
Molecular and Vascular Biology
Laboratory of Angiogenesis and Vascular Metabolism (Vesalius Research Center) (+)
# (joint) last author

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