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RECEPTORS AND SIGNAL TRANSDUCTION

Wnt/-catenin signaling activates growth-control genes during overload-induced skeletal muscle hypertrophy

¹University of Illinois Chicago, School of Kinesiology, Chicago, Illinois; and ²University of Kentucky, Department of Physiology, Lexington, Kentucky

Submitted 3 March 2005 ; accepted in final form 8 May 2005

-Catenin is a transcriptional activator shown to regulate the embryonic, postnatal, and oncogenic growth of many tissues. In most research to date, -catenin activation has been the unique downstream function of the Wnt signaling pathway. However, in the heart, a Wnt-independent mechanism involving Akt-mediated phosphorylation of glycogen synthase kinase (GSK)-3 was recently shown to activate -catenin and regulate cardiomyocyte growth. In this study, results have identified the activation of the Wnt/-catenin pathway during hypertrophy of mechanically overloaded skeletal muscle. Significant increases in -catenin were determined during skeletal muscle hypertrophy. In addition, the Wnt receptor, mFrizzled (mFzd)-1, the signaling mediator disheveled-1, and the transcriptional co-activator, lymphocyte enhancement factor (Lef)-1, are all increased during hypertrophy of the overloaded mouse plantaris muscle. Experiments also determined an increased association between GSK-3 and the inhibitory frequently rearranged in advanced T cell-1 protein with no increase in GSK-3 phosphorylation (Ser9). Finally, skeletal muscle overload resulted in increased nuclear -catenin/Lef-1 expression and induction of the transcriptional targets c-Myc, cyclin D1, and paired-like homeodomain transcription factor 2. Thus this study provides the first evidence that the Wnt signaling pathway induces -catenin/Lef-1 activation of growth-control genes during overload induced skeletal muscle hypertrophy.

lymphocyte enhancement factor-1; glycogen synthase kinase-3; paired like homeodomain transcription factor-2; c-Myc

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