Aging does not alter the mechanosensitivity of the p38, p70<sup>S6k</sup>, and JNK2 signaling pathways in skeletal muscle

Hornberger, Troy A.; Mateja, Ryan D.; Chin, Eva R.; Andrews, Jessica L.; Esser, Karyn A.

doi:10.1152/japplphysiol.00870.2004

Cited by 53 publications

(39 citation statements)

References 20 publications

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“…Maximum isometric tetanic force was determined in EDL muscles from mice [wild type (n = 4), Clock Δ19 (n = 7), Bmal1 −/− (n = 3), and MyoD −/− (n = 4)] following procedures described previously (43).…”

Section: Methodsmentioning

confidence: 99%

“…Skeletal muscle was homogenized in lysis buffer, and samples were electrophoresed on 10% SDS/PAGE and transferred to PVDF membrane (Millipore) as described previously (43). Membranes were incubated with a polyclonal antibody against MyoD (Santa Cruz Biotechnology) or γ-tubulin (Sigma-Aldrich) followed by incubation with alkaline phosphatase-linked anti-rabbit antibody or anti-mouse antibody (Sigma-Aldrich).…”

Section: Methodsmentioning

confidence: 99%

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CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function

Andrews

Zhang

McCarthy

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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319

341

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MyoD, a master regulator of myogenesis, exhibits a circadian rhythm in its mRNA and protein levels, suggesting a possible role in the daily maintenance of muscle phenotype and function. We report that MyoD is a direct target of the circadian transcriptional activators CLOCK and BMAL1, which bind in a rhythmic manner to the core enhancer of the MyoD promoter. Skeletal muscle of Clock Δ19 and Bmal1 −/− mutant mice exhibited ∼30% reductions in normalized maximal force. A similar reduction in force was observed at the single-fiber level. Electron microscopy (EM) showed that the myofilament architecture was disrupted in skeletal muscle of Clock Δ19 , Bmal1 −/− , and MyoD −/− mice. The alteration in myofilament organization was associated with decreased expression of actin, myosins, titin, and several MyoD target genes. EM analysis also demonstrated that muscle from both Clock Δ19 and Bmal1 −/− mice had a 40% reduction in mitochondrial volume. The remaining mitochondria in these mutant mice displayed aberrant morphology and increased uncoupling of respiration. This mitochondrial pathology was not seen in muscle of MyoD −/− mice. We suggest that altered expression of both Pgc-1α and Pgc-1β in Clock Δ19 and Bmal1 −/− mice may underlie this pathology. Taken together, our results demonstrate that disruption of CLOCK or BMAL1 leads to structural and functional alterations at the cellular level in skeletal muscle. The identification of MyoD as a clock-controlled gene provides a mechanism by which the circadian clock may generate a muscle-specific circadian transcriptome in an adaptive role for the daily maintenance of adult skeletal muscle.circadian clock | myofilaments | mitochondria A fundamental, evolutionarily conserved property of most organisms, from cyanobacteria to plants and animals, is the daily cycling of their internal physiology as well as certain behaviors in animals, such as sleep and feeding (1). The timing of these circadian rhythms is synchronized to the environment by external cues, with light and nutrient availability being two of the most salient entrainment cues (2). The synchronization of endogenous circadian rhythms with the daily cycles in the environment provides an adaptive mechanism for organisms to anticipate cyclic demands on cellular physiology and behavior (3, 4). At the molecular level, the circadian clock represents a well-defined gene regulatory network composed of transcriptional-translational feedback loops (5). The positive arm of the loop is composed of the transcription factors CLOCK and BMAL1, which heterodimerize and bind to E-box elements on target genes such as Per1 to drive the negative part of the feedback loop (5). More recently, the same molecular clock factors that have been identified in the central clock in the suprachiasmatic nucleus have been found to exist in most peripheral tissues (reviewed in ref. 6).We recently characterized the circadian transcriptome of adult skeletal muscle. These mRNAs exhibit significant oscillation in gene expression with a repeating period len...

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function

Andrews

Zhang

McCarthy

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

319

341

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“…Indeed, recent work showing increased p70 S6K phosphorylation with stretch activated mechanotransduction in skeletal muscle suggests that eccentric loading may be critical for S6K1 activation and therefore hypertrophy (Hornberger et al 2005a;Hornberger et al 2005b;Spangenburg and McBride 2006).…”

Section: A; Ruvinsky and Meyuhas 2006) Mammalian Cells Express Tmentioning

confidence: 99%

The Molecular Bases of Training Adaptation

2007

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“…It has been shown that mechanical stimulation activates p38 in muscle (Boppart et al, 2001;Hornberger et al, 2005) and in myoblasts that have undergone 2 days of differentiation (Rauch and Loughna, 2005). However, the mechanism whereby mechanical stimulation activates p38 in muscle cells Skeletal muscle responds to mechanical stimulation by activating p38 MAPK, a key signal for myogenesis.…”

Section: Introductionmentioning

confidence: 99%

TACE release of TNF-α mediates mechanotransduction-induced activation of p38 MAPK and myogenesis

Zhan

Jin

Chen

et al. 2007

Journal of Cell Science

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manner. Stretch stimulated the cleavage activity of TACE. Conversely, TACE inhibitor TAPI or TACE siRNA abolished stretch activation of p38. In addition, conditioned medium from stretched myoblast cultures activated p38 in unstretched myoblasts, which required TACE activity in the donor myoblasts, and TNF-␣ receptors in the recipient myoblasts. These results indicate that posttranscriptional activation of TACE mediates the mechanotransduction that activates p38-dependent myogenesis via the release of TNF-␣.

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Aging does not alter the mechanosensitivity of the p38, p70^S6k, and JNK2 signaling pathways in skeletal muscle

Cited by 53 publications

References 20 publications

CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function

CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function

The Molecular Bases of Training Adaptation

TACE release of TNF-α mediates mechanotransduction-induced activation of p38 MAPK and myogenesis

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Aging does not alter the mechanosensitivity of the p38, p70S6k, and JNK2 signaling pathways in skeletal muscle

Cited by 53 publications

References 20 publications

CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function

CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function

The Molecular Bases of Training Adaptation

TACE release of TNF-α mediates mechanotransduction-induced activation of p38 MAPK and myogenesis

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Aging does not alter the mechanosensitivity of the p38, p70^S6k, and JNK2 signaling pathways in skeletal muscle