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Inhibition of myostatin signaling through Notch activation following acute resistance exercise

MacKenzie, Matthew G, Hamilton, David Lee, Pepin, Mark, Patton, Amy and Baar, Keith 2013, Inhibition of myostatin signaling through Notch activation following acute resistance exercise, PLoS one, vol. 8, no. 7, pp. 1-7, doi: 10.1371/journal.pone.0068743.

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Title Inhibition of myostatin signaling through Notch activation following acute resistance exercise
Author(s) MacKenzie, Matthew G
Hamilton, David Lee
Pepin, Mark
Patton, Amy
Baar, Keith
Journal name PLoS one
Volume number 8
Issue number 7
Article ID e68743
Start page 1
End page 7
Total pages 7
Publisher Public Library of Science
Place of publication San Francisco, Calif.
Publication date 2013-07-02
ISSN 1932-6203
Keyword(s) blotting, western
hypertrophy
muscle proteins
myostatin
phosphorylation
receptors, Notch
reverse transcriptase polymerase chain reaction
signal transduction
SMAD2 protein
time factors
skeletal muscles
notching signaling
messenger RNA
gene expression
muscle differentiation
DNA transcription
SMAD signaling
signal inhibition
science & technology
Summary Myostatin is a TGFβ family member and negative regulator of muscle size. Due to the complexity of the molecular pathway between myostatin mRNA/protein and changes in transcription, it has been difficult to understand whether myostatin plays a role in resistance exercise-induced skeletal muscle hypertrophy. To circumvent this problem, we determined the expression of a unique myostatin target gene, Mighty, following resistance exercise. Mighty mRNA increased by 6 h (82.9 ± 24.21%) and remained high out to 48 h (56.5 ± 19.67%) after resistance exercise. Further examination of the soleus, plantaris and tibialis anterior muscles showed that the change in Mighty mRNA at 6 h correlated with the increase in muscle size associated with this protocol (R(2) = 0.9996). The increase in Mighty mRNA occurred both independent of Smad2 phosphorylation and in spite of an increase in myostatin mRNA (341.8 ± 147.14% at 3 h). The myostatin inhibitor SKI remained unchanged. However, activated Notch, another potential inhibitor of TGFβ signaling, increased immediately following resistance exercise (83 ± 11.2%) and stayed elevated out to 6 h (78 ± 16.6%). Electroportion of the Notch intracellular domain into the tibialis anterior resulted in an increase in Mighty mRNA (63 ± 13.4%) that was equivalent to the canonical Notch target HES-1 (94.4 ± 7.32%). These data suggest that acute resistance exercise decreases myostatin signaling through the activation of the TGFβ inhibitor Notch resulting in a decrease in myostatin transcriptional activity that correlates well with muscle hypertrophy.
Language eng
DOI 10.1371/journal.pone.0068743
Field of Research MD Multidisciplinary
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2013, MacKenzie et al.
Free to Read? Yes
Use Rights Creative Commons Attribution licence
Persistent URL http://hdl.handle.net/10536/DRO/DU:30112667

Document type: Journal Article
Collections: School of Life and Environmental Sciences
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.