Document Detail


Regulation of STARS and its downstream targets suggest a novel pathway involved in human skeletal muscle hypertrophy and atrophy.
MedLine Citation:
PMID:  19255118     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Skeletal muscle atrophy is a severe consequence of ageing, neurological disorders and chronic disease. Identifying the intracellular signalling pathways controlling changes in skeletal muscle size and function is vital for the future development of potential therapeutic interventions. Striated activator of Rho signalling (STARS), an actin-binding protein, has been implicated in rodent cardiac hypertrophy; however its role in human skeletal muscle has not been determined. This study aimed to establish if STARS, as well as its downstream signalling targets, RhoA, myocardin-related transcription factors A and B (MRTF-A/B) and serum response factor (SRF), were increased and decreased respectively, in human quadriceps muscle biopsies taken after 8 weeks of both hypertrophy-stimulating resistance training and atrophy-stimulating de-training. The mRNA levels of the SRF target genes involved in muscle structure, function and growth, such as alpha-actin, myosin heavy chain IIa (MHCIIa) and insulin-like growth factor-1 (IGF-1), were also measured. Following resistance training, STARS, MRTF-A, MRTF-B, SRF, alpha-actin, MHCIIa and IGF-1 mRNA, as well as RhoA and nuclear SRF protein levels were all significantly increased by between 1.25- and 3.6-fold. Following the de-training period all measured targets, except for RhoA, which remained elevated, returned to base-line. Our results show that the STARS signalling pathway is responsive to changes in skeletal muscle loading and appears to play a role in both human skeletal muscle hypertrophy and atrophy.
Authors:
Séverine Lamon; Marita A Wallace; Bertrand Léger; Aaron P Russell
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-03-02
Journal Detail:
Title:  The Journal of physiology     Volume:  587     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-04-16     Completed Date:  2009-07-15     Revised Date:  2010-09-23    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1795-803     Citation Subset:  IM    
Affiliation:
Clinique Romande de Réadaptation SUVA Care, Sion 1951, Switzerland.
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MeSH Terms
Descriptor/Qualifier:
Adult
Anaerobic Threshold / physiology
Atrophy
Blotting, Western
DNA Primers
DNA-Binding Proteins / physiology
Humans
Hypertrophy
Male
Microfilament Proteins / physiology*
Muscle, Skeletal / growth & development,  pathology,  physiology*
Oncogene Proteins, Fusion / physiology
Oxygen Consumption
Physical Endurance / physiology
Physical Fitness / physiology*
RNA, Messenger / biosynthesis,  genetics
Reverse Transcriptase Polymerase Chain Reaction
Serum Response Factor / physiology
Signal Transduction / physiology*
Tomography, X-Ray Computed
Transcription Factors / physiology*
Weight Lifting / physiology
Chemical
Reg. No./Substance:
0/ABRA protein, human; 0/DNA Primers; 0/DNA-Binding Proteins; 0/MKL1 protein, human; 0/Microfilament Proteins; 0/Oncogene Proteins, Fusion; 0/RNA, Messenger; 0/Serum Response Factor; 0/Transcription Factors
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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