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Originally published as MBC in Press, 10.1091/mbc.E04-08-0720 on January 26, 2005

Vol. 16, Issue 4, 2039-2048, April 2005

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Wnt10b Deficiency Promotes Coexpression of Myogenic and Adipogenic Programs in Myoblasts

Anthony M. Vertino *, Jane M. Taylor-Jones *, Kenneth A. Longo {dagger}, Edward D. Bearden *, Timothy F. Lane {ddagger}, Robert E. McGehee, Jr. §, Ormond A. MacDougald {dagger}, and Charlotte A. Peterson * || ¶

* Donald W. Reynolds Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72205; {dagger} Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109; {ddagger} Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA 90095; § Department of Pediatrics, Arkansas Children's Hospital and Arkansas Cancer Research Center, University of Arkansas for Medical Sciences, Little Rock, AR 72205; || Central Arkansas Veterans Health Care System, Little Rock, AR 72205; and Departments of Physiology and Biophysics and Orthopedic Surgery, University of Arkansas for Medical Sciences, Little Rock, AR 72205

Submitted August 19, 2004; Accepted January 18, 2005
Monitoring Editor: Marianne Bronner-Fraser

Adult myoblasts retain plasticity in developmental potential and can be induced to undergo myogenic, adipogenic, or osteoblastogenic differentiation in vitro. In this report, we show that the balance between myogenic and adipogenic potential in myoblasts is controlled by Wnt signaling. Furthermore, this balance is altered during aging such that aspects of both differentiation programs are coexpressed in myoblasts due to decreased Wnt10b abundance. Mimicking Wnt signaling in aged myoblasts through inhibition of glycogen synthase kinase or through overexpression of Wnt10b resulted in inhibition of adipogenic gene expression and sustained or enhanced myogenic differentiation. On the other hand, myoblasts isolated from Wnt10b null mice showed increased adipogenic potential, likely contributing to excessive lipid accumulation in actively regenerating myofibers in vivo in Wnt10b-/- mice. Whereas Wnt10b deficiency contributed to increased adipogenic potential in myoblasts, the augmented myogenic differentiation potential observed is likely the result of a compensatory increase in Wnt7b during differentiation of Wnt10b-/- myoblasts. No such compensation was apparent in aged myoblasts and in fact, both Wnt5b and Wnt10b were down-regulated. Thus, alteration in Wnt signaling in myoblasts with age may contribute to impaired muscle regenerative capacity and to increased muscle adiposity, both characteristic of aged muscle.

This article was published online ahead of print in MBC in Press (http://www.molbiolcell.org/cgi/doi/10.1091/mbc.E04-08-0720) on January 26, 2005.

Abbreviations used: C/EBP{alpha}, CAAT/enhancer binding protein {alpha}; DM, differentiation medium; FABP4, fatty acid binding protein 4; GM, growth medium; GSK, glycogen synthase kinase; IBMX, 3-isobutyl-1-methylxanthine; PPAR{gamma}, peroxisome proliferator-activated receptor {gamma}; RT-PCR, reverse transcriptase-polymerase chain reaction; TCF, T cell factor.

Address correspondence to: Charlotte A. Peterson (PetersonCharlotteA{at}uams.edu).




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