Modulating skeletal muscle mass by postnatal, muscle-specific inactivation of the myostatin gene.
By using a conditional gene targeting approach exploiting the cre-lox system, we show that postnatal inactivation of the myostatin gene in striated muscle is sufficient to cause a generalized muscular hypertrophy of the same magnitude as that observed for constitutive myostatin knockout mice. This formally demonstrates that striated muscle is the production site of functional myostatin and that this member of the TGFbeta family of growth and differentiation factors regulates muscle mass not only during early embryogenesis but throughout development. It indicates that myostatin antagonist could be used to treat muscle wasting and to promote muscle growth in man and animals.
Grobet
Luc
L
Department of Genetics, Faculty of Veterinary Medicine, University of Liège (B43), 20 Boulevard de Colonster, B-4000 Liège, Belgium.
Pirottin
Dimitri
D
Farnir
Frédéric
F
Poncelet
Dominique
D
Royo
Luis Jose
LJ
Brouwers
Benoît
B
Christians
Elisabeth
E
Desmecht
Daniel
D
Coignoul
Freddy
F
Kahn
Ronald
R
Georges
Michel
M
D000818:Animals; D003433:Crosses, Genetic; D019426:Integrases / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008822:Mice, Transgenic; D018482:Muscle, Skeletal / Q000378:metabolism*; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism*; D014764:Viral Proteins / Q000235:genetics / Q000378:metabolism
D016212:Transforming Growth Factor beta; D014764:Viral Proteins; C045073:Cre recombinase; D019426:Integrases