Inhibition of myostatin signaling through Notch activation following acute resistance exercise.

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 hyper...

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Autores principales:	Matthew G MacKenzie, David Lee Hamilton, Mark Pepin, Amy Patton, Keith Baar
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/26c7e481c8af415cbfd442009040a432
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spelling	oai:doaj.org-article:26c7e481c8af415cbfd442009040a4322021-11-18T07:38:56ZInhibition of myostatin signaling through Notch activation following acute resistance exercise.1932-620310.1371/journal.pone.0068743https://doaj.org/article/26c7e481c8af415cbfd442009040a4322013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23844238/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Myostatin 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.Matthew G MacKenzieDavid Lee HamiltonMark PepinAmy PattonKeith BaarPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 7, p e68743 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Matthew G MacKenzie David Lee Hamilton Mark Pepin Amy Patton Keith Baar Inhibition of myostatin signaling through Notch activation following acute resistance exercise.
description	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.
format	article
author	Matthew G MacKenzie David Lee Hamilton Mark Pepin Amy Patton Keith Baar
author_facet	Matthew G MacKenzie David Lee Hamilton Mark Pepin Amy Patton Keith Baar
author_sort	Matthew G MacKenzie
title	Inhibition of myostatin signaling through Notch activation following acute resistance exercise.
title_short	Inhibition of myostatin signaling through Notch activation following acute resistance exercise.
title_full	Inhibition of myostatin signaling through Notch activation following acute resistance exercise.
title_fullStr	Inhibition of myostatin signaling through Notch activation following acute resistance exercise.
title_full_unstemmed	Inhibition of myostatin signaling through Notch activation following acute resistance exercise.
title_sort	inhibition of myostatin signaling through notch activation following acute resistance exercise.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/26c7e481c8af415cbfd442009040a432
work_keys_str_mv	AT matthewgmackenzie inhibitionofmyostatinsignalingthroughnotchactivationfollowingacuteresistanceexercise AT davidleehamilton inhibitionofmyostatinsignalingthroughnotchactivationfollowingacuteresistanceexercise AT markpepin inhibitionofmyostatinsignalingthroughnotchactivationfollowingacuteresistanceexercise AT amypatton inhibitionofmyostatinsignalingthroughnotchactivationfollowingacuteresistanceexercise AT keithbaar inhibitionofmyostatinsignalingthroughnotchactivationfollowingacuteresistanceexercise
_version_	1718423149120323584

Inhibition of myostatin signaling through Notch activation following acute resistance exercise.

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