Contractile activity attenuates autophagy suppression and reverses mitochondrial defects in skeletal muscle cells

Parousis, A.; Carter, Heather N.; Tran, Claudia; Erlich, Avigail T.; Moosavi, Zahra S. Mesbah; Pauly, Marion; Hood, David A.

doi:10.1080/15548627.2018.1491488

Cited by 43 publications

(22 citation statements)

References 74 publications

(89 reference statements)

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“…It is possible that this short duration of heat is increasing initiation signals, without inducing high levels of cellular stress that would further drive autophagic flux, as supported by reduction in p38 and JNK phosphorylation, and no change in NF-κB signaling. Our finding is consistent with the effects of both muscle contraction and exercise to reduce autophagasome accumulation in the presence of chemical inhibition of autophagy, despite increased basal levels of autophagy (Jiang et al, 2014;Parousis et al, 2018). This effect is speculated to reflect a normalization of autophagic degradation, although the mechanism underlying this effect remains unclear.…”

Section: Discussionsupporting

confidence: 89%

Acute Heat Exposure Alters Autophagy Signaling in C2C12 Myotubes

Summers

Valentine

2020

Front. Physiol.

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Autophagy is a major intracellular degradation process that is essential for the clearance of unnecessary proteins/organelles and the maintenance of cellular homeostasis. The inhibition of autophagy results in cellular consequences associated with many skeletal muscle pathologies, and therapies designed to elevate autophagic activity may provide protection from such pathologies. Acute exposure to low levels of heat has therapeutic effects; however, the impact of heat on skeletal muscle autophagy remains unclear. In the present study, C2C12 myotubes were maintained at 37 • C thermoneutral (TN) or heated at 40 • C heat treatment (HT) for 1 h. Myotubes were harvested immediately after heating, or returned to 37 • C for recovery of 2 or 24 h. HT resulted in an elevation in pAMPK (T172), Beclin-1, and LC3 II, a marker for autophagosome formation, but no change in p62. In the context of autophagy inhibition with Bafilomycin A1, HT resulted in lower LC3 II compared to TN. The applied heat load induced the heat shock response, as evidenced by immediate upregulation of HSF1 and Hsp70. Hsp70 continued to increase during recovery, whereas pHsp27 was downregulated acutely in response to HT, but retuned to TN levels by 2 h of recovery. HT also reduced the phosphorylation of the MAP-kinases p38 and JNK. These findings suggest that an acute, short bout of mild heat may be beneficial to skeletal muscle by increasing AMPK activity, markers of autophagasome formation, and the heat shock response.

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Section: Discussionsupporting

confidence: 89%

Acute Heat Exposure Alters Autophagy Signaling in C2C12 Myotubes

Summers

Valentine

2020

Front. Physiol.

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“…) and chronic contractile activity (Parousis et al . ), and we also observed elevated protein levels during postnatal period (Fig. A ).…”

Section: Discussionsupporting

confidence: 75%

Protein composition of the muscle mitochondrial reticulum during postnatal development

Kim

Yang

Katti

2019

The Journal of Physiology

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Key pointsr Muscle mitochondrial networks changed from a longitudinal, fibre parallel orientation to a perpendicular configuration during postnatal development.r Mitochondrial dynamics, mitophagy and calcium uptake proteins were abundant during early postnatal development.r Mitochondrial biogenesis and oxidative phosphorylation proteins were upregulated throughout muscle development.r Postnatal muscle mitochondrial network formation is accompanied by a change in protein expression profile from mitochondria designed for co-ordinated cellular assembly to mitochondria highly specialized for cellular energy metabolism.Abstract Striated muscle mitochondria form connected networks capable of rapid cellular energy distribution. However, the mitochondrial reticulum is not formed at birth and the mechanisms driving network development remain unclear. In the present study, we aimed to establish the network formation timecourse and protein expression profile during postnatal development of the murine muscle mitochondrial reticulum. Two-photon microscopy was used to observe mitochondrial network orientation in tibialis anterior (TA) muscles of live mice at postnatal days (P) 1, 7, 14, 21 and 42, respectively. All muscle fibres maintained a longitudinal, fibre parallel mitochondrial network orientation early in development (P1-7). Mixed networks were most common at P14 but, by P21, almost all fibres had developed the perpendicular mitochondrial orientation observed in mature, glycolytic fibres. Tandem mass tag proteomics were then applied to examine changes in 6869 protein abundances in developing TA muscles. Mitochondrial proteins increased by 32% from P1 to P42. In addition, both nuclear-and mitochondrial-DNA encoded oxidative phosphorylation (OxPhos) components were increased during development, whereas OxPhos assembly factors decreased. Although mitochondrial dynamics and mitophagy were induced at P1-7, mitochondrial biogenesis was enhanced after P14. Moreover, calcium signalling Y. Kim and others J Physiol 597.10 proteins and the mitochondrial calcium uniporter had the highest expression early in postnatal development. In conclusion, mitochondrial networks transform from a fibre parallel to perpendicular orientation during the second and third weeks after birth in murine glycolytic skeletal muscle. This structural transition is accompanied by a change in protein expression profile from mitochondria designed for co-ordinated cellular assembly to mitochondria highly specialized for cellular energy metabolism.

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“…This figure is available as part of a downloadable slideset -independent mechanisms [29], optimising insulin action and both glucose oxidation and storage. Continuation of regular exercise further augments skeletal muscle oxidative capacity, mitochondrial biogenesis [30] and mitochondrial quality control mechanisms (mitophagy, fission, fusion), although this has been less well examined [31,32]. Endurance training promotes the trafficking of dietary fatty acids away from storage and towards oxidation via an increased capacity for myocyte fatty acid transport paired with increased fatty acid oxidation in mitochondria in both normal weight and overweight adults [33].…”

Section: Muscle-centric Vs Integrative View Of the Impact Of Exercisementioning

confidence: 99%

Exercise and metabolic health: beyond skeletal muscle

2020

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Regular exercise is a formidable regulator of insulin sensitivity and overall systemic metabolism through both acute events driven by each exercise bout and through chronic adaptations. As a result, regular exercise significantly reduces the risks for chronic metabolic disease states, including type 2 diabetes and non-alcoholic fatty liver disease. Many of the metabolic health benefits of exercise depend on skeletal muscle adaptations; however, there is plenty of evidence that exercise exerts many of its metabolic benefit through the liver, adipose tissue, vasculature and pancreas. This review will highlight how exercise reduces metabolic disease risk by activating metabolic changes in non-skeletal-muscle tissues. We provide an overview of exercise-induced adaptations within each tissue and discuss emerging work on the exercise-induced integration of inter-tissue communication by a variety of signalling molecules, hormones and cytokines collectively named 'exerkines'. Overall, the evidence clearly indicates that exercise is a robust modulator of metabolism and a powerful protective agent against metabolic disease, and this is likely to be because it robustly improves metabolic function in multiple organs.

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Contractile activity attenuates autophagy suppression and reverses mitochondrial defects in skeletal muscle cells

Cited by 43 publications

References 74 publications

Acute Heat Exposure Alters Autophagy Signaling in C2C12 Myotubes

Acute Heat Exposure Alters Autophagy Signaling in C2C12 Myotubes

Protein composition of the muscle mitochondrial reticulum during postnatal development

Exercise and metabolic health: beyond skeletal muscle

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