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Blood, 15 March 2001, Vol. 97, No. 6, pp. 1703-1711
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Urokinase-dependent plasminogen activation is required for
efficient skeletal muscle regeneration in vivo
Frederic Lluís,
Josep Roma,
Mònica Suelves,
Maribel Parra,
Gloria Aniorte,
Eduard Gallardo,
Isabel Illa,
Luciano Rodríguez,
Simon M. Hughes,
Peter Carmeliet,
Manuel Roig, and
Pura Muñoz-Cánoves
From the Centre d'Oncologia Molecular, Institut de
Recerca Oncològica; the Unitat de Recerca de la Vall d'Hebron;
the Hospital de la Santa Creu i Sant Pau, Barcelona, Spain; the Center
for Transgene Technology, Flanders Interuniversity, Leuven, Belgium;
and the Randall Centre, New Hunt's House, Kings College, London,
United Kingdom.
Plasminogen activators urokinase-type plasminogen activator (uPA)
and tissue-type plasminogen activator (tPA) are extracellular proteases
involved in various tissue remodeling processes. A requirement for uPA
activity in skeletal myogenesis was recently demonstrated in vitro. The
role of plasminogen activators in skeletal muscle regeneration in vivo
in wild-type, uPA-deficient, and tPA-deficient mice is investigated
here. Wild-type and tPA / mice completely repaired experimentally
damaged skeletal muscle. In contrast, uPA/ mice had a severe
regeneration defect, with decreased recruitment of blood-derived
monocytes to the site of injury and with persistent myotube
degeneration. In addition, uPA-deficient mice accumulated fibrin in the
degenerating muscle fibers; however, the defibrinogenation of
uPA-deficient mice resulted in a correction of the muscle regeneration defect. A similar severe regeneration deficit with persistent fibrin
deposition was also reproducible in plasminogen-deficient mice after
injury, suggesting that fibrinolysis by uPA-mediated plasminogen
activation plays a fundamental role in skeletal muscle regeneration. In
conclusion, the uPA-plasmin system is identified as a critical
component of the mammalian skeletal muscle regeneration process,
possibly because it prevents intramuscular fibrin accumulation and
contributes to the adequate inflammatory response after injury. These
studies demonstrate the requirement of an extracellular proteolytic
cascade during muscle regeneration in vivo.
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