RGD Reference Report - Changes in skeletal muscle and tendon structure and function following genetic inactivation of myostatin in rats. - Rat Genome Database

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Changes in skeletal muscle and tendon structure and function following genetic inactivation of myostatin in rats.

Authors: Mendias, Christopher L  Lynch, Evan B  Gumucio, Jonathan P  Flood, Michael D  Rittman, Danielle S  Van Pelt, Douglas W  Roche, Stuart M  Davis, Carol S 
Citation: Mendias CL, etal., J Physiol. 2015 Apr 15;593(8):2037-52. doi: 10.1113/jphysiol.2014.287144. Epub 2015 Feb 25.
RGD ID: 151347429
Pubmed: PMID:25640143   (View Abstract at PubMed)
PMCID: PMC4405758   (View Article at PubMed Central)
DOI: DOI:10.1113/jphysiol.2014.287144   (Journal Full-text)

Myostatin is a negative regulator of skeletal muscle and tendon mass. Myostatin deficiency has been well studied in mice, but limited data are available on how myostatin regulates the structure and function of muscles and tendons of larger animals. We hypothesized that, in comparison to wild-type (MSTN(+/+) ) rats, rats in which zinc finger nucleases were used to genetically inactivate myostatin (MSTN(Δ/Δ) ) would exhibit an increase in muscle mass and total force production, a reduction in specific force, an accumulation of type II fibres and a decrease and stiffening of connective tissue. Overall, the muscle and tendon phenotype of myostatin-deficient rats was markedly different from that of myostatin-deficient mice, which have impaired contractility and pathological changes to fibres and their extracellular matrix. Extensor digitorum longus and soleus muscles of MSTN(Δ/Δ) rats demonstrated 20-33% increases in mass, 35-45% increases in fibre number, 20-57% increases in isometric force and no differences in specific force. The insulin-like growth factor-1 pathway was activated to a greater extent in MSTN(Δ/Δ) muscles, but no substantial differences in atrophy-related genes were observed. Tendons of MSTN(Δ/Δ) rats had a 20% reduction in peak strain, with no differences in mass, peak stress or stiffness. The general morphology and gene expression patterns were similar between tendons of both genotypes. This large rodent model of myostatin deficiency did not have the negative consequences to muscle fibres and extracellular matrix observed in mouse models, and suggests that the greatest impact of myostatin in the regulation of muscle mass may not be to induce atrophy directly, but rather to block hypertrophy signalling.



Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
MstnRatincreased body weight  IMP compared to wild typeRGD 
Mstnem1McwiRatincreased body weight  IMP compared to wild typeRGD 
SS-Mstnem1Mcwi-/-Ratincreased body weight  IMP compared to wild typeRGD 
MstnRatincreased skeletal muscle fiber size  IMP compared to wild typeRGD 
Mstnem1McwiRatincreased skeletal muscle fiber size  IMP compared to wild typeRGD 
SS-Mstnem1Mcwi-/-Ratincreased skeletal muscle fiber size  IMP compared to wild typeRGD 
MstnRatincreased skeletal muscle mass  IMP compared to wild typeRGD 
Mstnem1McwiRatincreased skeletal muscle mass  IMP compared to wild typeRGD 
SS-Mstnem1Mcwi-/-Ratincreased skeletal muscle mass  IMP compared to wild typeRGD 
Objects Annotated

Genes (Rattus norvegicus)
Mstn  (myostatin)
Mstnem1Mcwi  (myostatin; zinc finger nuclease induced mutant 1, Medical College of Wisconsin)

Strains
SS-Mstnem1Mcwi-/-  (SS-Mstnem1Mcwi-/Mstnem1Mcwi-)


Additional Information