| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 University of Rochester Medical Center
* To whom correspondence should be addressed. E-mail: stephen_welle{at}urmc.rochester.edu.
Knocking out myostatin activity during development increases the rate of muscle protein synthesis. The present study was done to determine whether postdevelopmental loss of myostatin activity stimulates myofibrillar protein synthesis and the phosphorylation of some of the proteins involved in regulation of protein synthesis rate. Myostatin activity was inhibited for 4 days, in 4-5 month old male mice, with injections of an anti-myostatin antibody (JA16). The mean myofibrillar synthesis rate increased 19% (P < 0.01) relative to the mean rate in saline-treated mice, as determined by incorporation of deuterium-labeled phenylalanine. JA16 increased phosphorylation of p70 S6 kinase (S6K) and ribosomal protein S6 (rpS6) 1.9-fold (P < 0.05). It did not affect phosphorylation of eukaryotic initiation factor 4E binding protein-1 or Akt. Microarrays and real-time PCR analyses indicated that JA16 administration did not selectively enrich levels of mRNAs encoding myofibrillar proteins, ribosomal proteins, or translation initiation and elongation factors. Rapamycin treatment did not affect the rate of myofibrillar protein synthesis whether or not the mice received JA16 injections, even though it eliminated the phosphorylation of S6K and rpS6. We conclude that the normal level of myostatin activity in mature muscle is sufficient to inhibit myofibrillar synthesis rate and phosphorylation of S6K and rpS6. Reversal of the inhibition of myofibrillar synthesis with an anti-myostatin antibody is not dependent on mTOR activation.
This article has been cited by other articles:
|
|
 |
|
  M. R. Morissette, S. A. Cook, C. Buranasombati, M. A. Rosenberg, and A. Rosenzweig Myostatin inhibits IGF-I-induced myotube hypertrophy through Akt Am J Physiol Cell Physiol, November 1, 2009; 297(5): 1124 - 1132. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Welle, K. Burgess, C. A. Thornton, and R. Tawil Relation between extent of myostatin depletion and muscle growth in mature mice Am J Physiol Endocrinol Metab, October 1, 2009; 297(4): E935 - E940. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Welle, A. Cardillo, M. Zanche, and R. Tawil Skeletal muscle gene expression after myostatin knockout in mature mice Physiol Genomics, August 7, 2009; 38(3): 342 - 350. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Gilson, O. Schakman, S. Kalista, P. Lause, K. Tsuchida, and J.-P. Thissen Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin Am J Physiol Endocrinol Metab, July 1, 2009; 297(1): E157 - E164. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Sartori, G. Milan, M. Patron, C. Mammucari, B. Blaauw, R. Abraham, and M. Sandri Smad2 and 3 transcription factors control muscle mass in adulthood Am J Physiol Cell Physiol, June 1, 2009; 296(6): C1248 - C1257. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. L. Welle Myostatin and muscle fiber size. Focus on "Smad2 and 3 transcription factors control muscle mass in adulthood" and "Myostatin reduces Akt/TORC1/p70S6K signaling, inhibiting myoblast differentiation and myotube size" Am J Physiol Cell Physiol, June 1, 2009; 296(6): C1245 - C1247. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
