Altering aspects of mitochondrial quality to improve musculoskeletal outcomes in disuse atrophy---Supplementary Figure 8
Figures are generally photos, graphs and static images that would be represented in traditional pdf publications.
Figure 8: mRNA content of markers of mitophagy and
fatty acid oxidation in the soleus muscle of MCAT mice. A: Pparα
mRNA content in males. B: Pparα
mRNA content in females. C: Bnip3 mRNA content in males. D:
Bnip3 mRNA content in females. Larger graphs are the responses of WT-HU
and MCAT-HU, with the inset graph containing comparisons between WT-CON and
MCAT-CON. To demonstrate responses compared to control, 1 (indicating the
within genotype basal levels) is graphed with a dotted line. * = p<0.05 from a Student’s T-test
between genotypes. Males had the following sample sizes: WT-CON= 8, WT-HU= 7,
MCAT-CON= 4, MCAT-HU= 3. Females had the following samples sizes: WT-CON= 5,
WT-HU= 6, MCAT-CON= 6, MCAT-HU= 6.
Article Title: Altering aspects of mitochondrial quality to improve musculoskeletal outcomes in disuse atrophy
Authors: Megan E. Rosa-Caldwell, Seongkyun Lim, Wesley S. Haynie, Lisa T. Jansen, Lauren C. Westervelt, Madeline G. Amos, Tyrone A. Washington, Nicholas P. Greene
Abstract: Muscle atrophy is a significant moderator for disease prognosis; as such, interventions to mitigate disuse-induced muscle loss are imperative to improve clinical interventions. Mitochondrial deteriorations may underlie disuse-induced myopathies; therefore, improving mitochondrial quality may be an enticing therapeutic intervention. However, different mitochondrial-based treatments may have divergent impacts on the prognosis of disuse atrophy. Therefore, the purpose of this study was to investigate different mitochondria-centered interventions during disuse atrophy in hindlimb unloaded male and female mice. Methods: Male and female mice overexpressing PGC-1α (PGC-1α) or mitochondrially-targeted catalase (MCAT) and their respective wildtype (WT) littermate controls were hindlimb unloaded for 7 days to induce disuse atrophy or allowed normal ambulatory activity (cage control; CON). After designated interventions, animals were euthanized and tissues collected for measures of mitochondrial quality control and protein turnover. Results: While PGC-1α overexpression mitigated ubiquitin-proteasome activation (MuRF1 and Atrogin mRNA content), this did not correspond to phenotypic protections from disuse-induced atrophy. Rather, PGC-1α mice appeared to have a greater reliance on autophagic protein breakdown compared to WT. In MCAT mice, females exhibited a mitigated response to disuse atrophy; however, this effect was not noted in males. Despite these phenotypic differences, there were no clear cellular signaling differences between MCAT hindlimb unloaded females and MCAT fully loaded females. Conclusion: PGC-1α overexpression does not protect against phenotypic alterations during disuse atrophy but appears to shift catabolic pathways moderating atrophy. However, increased mitochondrially-targeted catalase activity appears to blunt disuse atrophy within highly oxidative muscles specifically in female mice.
Mitochondrial Degeneration ? the Root of Skeletal Muscle Atrophy
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