Am J Physiol Cell Physiol Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol (May 11, 2005). doi:10.1152/ajpcell.00093.2005
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
289/4/C853    most recent
00093.2005v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Armstrong, D. D
Right arrow Articles by Esser, K. A
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Armstrong, D. D
Right arrow Articles by Esser, K. A
Submitted on March 3, 2005
Accepted on May 8, 2005

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

Dustin D Armstrong1 and Karyn A Esser1*

1 Kinesiology, University of Illinois, Chicago, Chicago, IL, USA; Physiology, University of Kentucky, Lexington, KY, USA

* To whom correspondence should be addressed. E-mail: karyn.esser{at}uky.edu.

{beta}-catenin is a transcriptional activator shown to regulate the embryonic, postnatal, and oncogenic growth of many tissues. In most research to date, {beta}-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 GSK-3{beta} was recently shown to activate {beta}-catenin and regulate cardiomyocyte growth. In this study, results have identified the activation of the Wnt/{beta}-catenin pathway during hypertrophy of mechanically overloaded skeletal muscle. Significant increases in {beta}-catenin were determined during skeletal muscle hypertrophy. In addition, the Wnt-receptor, mFrizzled-1, the signaling mediator Dishevelled-1, and the transcriptional co-activator, Lef-1, are all increased during hypertrophy of the overloaded mouse plantaris muscle. Experiments also determined an increased association between GSK-3{beta} and the inhibitory Frat1 protein with no increase in GSK-3{beta} phosphorylation (ser9). Finally, skeletal muscle overload resulted in increased nuclear {beta}-catenin/Lef-1 expression and induction of the transcriptional targets c-Myc, Cyclin D1 and Pitx2. Thus, this study provides the first evidence that the Wnt signaling pathway induces {beta}-catenin/Lef-1 activation of growth-control genes during overload induced skeletal muscle hypertrophy.




This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
M. Miyazaki and K. A. Esser
Cellular mechanisms regulating protein synthesis and skeletal muscle hypertrophy in animals
J Appl Physiol, April 1, 2009; 106(4): 1367 - 1373.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
J. F. Tong, X. Yan, M. J. Zhu, S. P. Ford, P. W. Nathanielsz, and M. Du
Maternal obesity downregulates myogenesis and {beta}-catenin signaling in fetal skeletal muscle
Am J Physiol Endocrinol Metab, April 1, 2009; 296(4): E917 - E924.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
J. K. Bentley, H. Deng, M. J. Linn, J. Lei, G. A. Dokshin, D. C. Fingar, K. N. Bitar, W. R. Henderson Jr., and M. B. Hershenson
Airway smooth muscle hyperplasia and hypertrophy correlate with glycogen synthase kinase-3{beta} phosphorylation in a mouse model of asthma
Am J Physiol Lung Cell Mol Physiol, February 1, 2009; 296(2): L176 - L184.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
M. G. MacKenzie, D. L. Hamilton, J. T. Murray, P. M. Taylor, and K. Baar
mVps34 is activated following high-resistance contractions
J. Physiol., January 1, 2009; 587(1): 253 - 260.
[Abstract] [Full Text] [PDF]

Home page
 FASEB J.Home page
H. E. MacLean, W. S. M. Chiu, A. J. Notini, A.-M. Axell, R. A. Davey, J. F. McManus, C. Ma, D. R. Plant, G. S. Lynch, and J. D. Zajac
Impaired skeletal muscle development and function in male, but not female, genomic androgen receptor knockout mice
FASEB J, August 1, 2008; 22(8): 2676 - 2689.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
J. L. J. van der Velden, R. C. J. Langen, M. C. J. M. Kelders, J. Willems, E. F. M. Wouters, Y. M. W. Janssen-Heininger, and A. M. W. J. Schols
Myogenic differentiation during regrowth of atrophied skeletal muscle is associated with inactivation of GSK-3beta
Am J Physiol Cell Physiol, May 1, 2007; 292(5): C1636 - C1644.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
T. Brade, J. Manner, and M. Kuhl
The role of Wnt signalling in cardiac development and tissue remodelling in the mature heart
Cardiovasc Res, November 1, 2006; 72(2): 198 - 209.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
D. D. Armstrong, V. L. Wong, and K. A. Esser
Expression of beta-catenin is necessary for physiological growth of adult skeletal muscle
Am J Physiol Cell Physiol, July 1, 2006; 291(1): C185 - C188.
[Abstract] [Full Text] [PDF]

Home page
 DevelopmentHome page
P. W. Heiser, J. Lau, M. M. Taketo, P. L. Herrera, and M. Hebrok
Stabilization of {beta}-catenin impacts pancreas growth
Development, May 15, 2006; 133(10): 2023 - 2032.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1977 by the American Physiological Society.