Projects per year
Abstract
Although the signal pathways mediating muscle protein synthesis and degradation are well characterized, the transcriptional processes modulating skeletal muscle mass and adaptive growth are poorly understood. Recently, studies in mouse models of muscle wasting or acutely exercised human muscle have suggested a potential role for the transcription factor, signal transducer and activator of transcription 3 (STAT3), in adaptive growth. Hence, in the present study we sought to define the contribution of STAT3 to skeletal muscle adaptive growth. In contrast to previous work, two different resistance exercise protocols did not change STAT3 phosphorylation in human skeletal muscle. To directly address the role of STAT3 in load-induced (i.e. adaptive) growth, we studied the anabolic effects of 14 days of synergist ablation (SA) in skeletal muscle-specific STAT3 knockout (mKO) mice and their floxed, wild type (WT) littermates. Plantaris muscle weight and fibre area in the non-operated leg (Control; CON) was comparable between genotypes. As expected, SA significantly increased plantaris weight, muscle fibre cross sectional area and anabolic signalling in WT mice, although interestingly, this induction was not impaired in STAT3 mKO mice. Collectively, these data demonstrate that STAT3 is not required for overload-mediated hypertrophy in mouse skeletal muscle.
Original language | English |
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Pages (from-to) | C257-C261 |
Journal | AJP: Cell Physiology |
Volume | 313 |
Issue number | 3 |
DOIs | |
Publication status | Published - 28 Jun 2017 |
Keywords
- hypertrophy
- resistance exercise
- STAT3
- skeletal muscle
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- 2 Finished
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Activating mitochondrial biogenesis in skeletal muscle through repression of the acetyltransferase GCN5.
Philp, A. (Principal Investigator)
Biotechnology & Biological Sciences Research Council
19/01/15 → 18/01/18
Project: Research Councils
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Determining the function of the transcriptional co-repressor RIP140 in skeletal muscle metabolic adaptation to exercise and insulin resistance
Perez-Schindler, J. (Principal Investigator) & Philp, A. (Co-Investigator)
1/01/14 → 31/12/17
Project: Research