|Appears in Collections:||Faculty of Health Sciences and Sport Journal Articles|
|Peer Review Status:||Refereed|
|Title:||Inhibition of Myostatin Signaling through Notch Activation following Acute Resistance Exercise|
|Author(s):||MacKenzie, Matthew G|
Hamilton, David Lee
|Citation:||MacKenzie MG, Hamilton DL, Pepin M, Patton A & Baar K (2013) Inhibition of Myostatin Signaling through Notch Activation following Acute Resistance Exercise, PLoS ONE, 8 (7), Art. No.: e68743.|
|Abstract:||Myostatin is a TGFb 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 (82.9624.21%) and remained high out to 48 h (56.5619.67%) 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 (R2 = 0.9996). The increase in Mighty mRNA occurred both independent of Smad2 phosphorylation and in spite of an increase in myostatin mRNA (341.86147.14% at 3 h). The myostatin inhibitor SKI remained unchanged. However, activated Notch, another potential inhibitor of TGFb signaling, increased immediately following resistance exercise (83611.2%) and stayed elevated out to 6 h (78616.6%). Electroportion of the Notch intracellular domain into the tibialis anterior resulted in an increase in Mighty mRNA (63613.4%) that was equivalent to the canonical Notch target HES-1 (94.467.32%). These data suggest that acute resistance exercise decreases myostatin signaling through the activation of the TGFb inhibitor Notch resulting in a decrease in myostatin transcriptional activity that correlates well with muscle hypertrophy.|
|Rights:||Copyright 2013 MacKenzie et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
|Mackenzie, Hamilton et al, 2013..pdf||864.6 kB||Adobe PDF||View/Open|
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