Document Detail


Lack of Smad3 signaling leads to impaired skeletal muscle regeneration.
MedLine Citation:
PMID:  22535746     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Smad3 is a key intracellular signaling mediator for both TGF-β and Myostatin, two major regulators of skeletal muscle growth. Previous published work has revealed pronounced muscle atrophy together with impaired Satellite Cell (SC) functionality in Smad3-null muscles. In the present study, we have further validated a role for Smad3 signaling in skeletal muscle regeneration. Here, we show that Smad3-null mice had incomplete recovery of muscle weight and myofiber size after muscle injury. Histological/Immunohistochemical analysis suggested impaired inflammatory response and reduced number of activated myoblasts during the early stages of muscle regeneration in the M. tibialis anterior muscle of Smad3-null mice. Nascent myofibers formed after muscle injury were also reduced in number. Moreover, Smad3-null regenerated muscle had decreased oxidative enzyme activity and impaired mitochondrial biogenesis, evident by the down-regulation of the gene encoding TFAM, a master regulator of mitochondrial biogenesis. Consistent with known Smad3 function, reduced fibrotic tissue formation was also seen in regenerated Smad3-null muscle. In conclusion, Smad3 deficiency leads to impaired muscle regeneration, which underscores an essential role of Smad3 in post-natal myogenesis. Given the negative role of Myostatin during muscle regeneration, the increased expression of Myostatin observed in Smad3-null muscle may contribute to the regeneration defects.
Authors:
Xiaojia Ge; Anuradha Vajjala; Craig McFarlane; Walter Wahli; Mridula Sharma; Ravi Kambadur
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-4-24
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  -     ISSN:  1522-1555     ISO Abbreviation:  -     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-4-26     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
1Nanyang Technological University.
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