Exercise training increases the expression and nuclear localization of mRNA destabilizing proteins in skeletal muscle

Matravadia, Sarthak; Martino, Vanessa; Sinclair, Daniel; Mutch, David M.; Holloway, Graham P.

doi:10.1152/ajpregu.00590.2012

Cited by 9 publications

(6 citation statements)

References 50 publications

(54 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Quantitative real-time PCR RNA isolation and analysis was performed as previously described [25]. See the electronic supplementary material (ESM) for further details.…”

Section: Methodsmentioning

confidence: 99%

In adipose tissue, increased mitochondrial emission of reactive oxygen species is important for short-term high-fat diet-induced insulin resistance in mice

et al. 2015

Self Cite

View full text Add to dashboard Cite

Aims/hypothesis Consuming a high-fat diet (HFD) induces insulin resistance in white adipose tissue (WAT) within 1 week. However, little is known about the initiating events. One potential mechanism that has remained largely unexplored is excessive mitochondrial emission of reactive oxygen species (ROS). Methods To determine the role of mitochondrial ROS emissions at the onset of insulin resistance, wild-type (WT) mice were placed on an HFD for 1 week. WAT insulin sensitivity and inflammation were assessed by western blot. In addition, we optimised/validated a method to determine ROS emissions in permeabilised WAT. Results An HFD for 1 week resulted in impaired insulin signalling, increased c-Jun NH 2 -terminal kinase (JNK) phosphorylation and an increase in oxidative stress. These changes were associated with an increase in fatty-acid-mediated mitochondrial ROS emissions without any change in mitochondrial respiration/content. To determine that mitochondrial ROS causes insulin resistance, we used transgenic mice that express human catalase in mitochondria (MCAT) as a model of upregulated mitochondrial antioxidant enzyme capacity. MCAT mice displayed attenuated mitochondrial ROS emission, preserved insulin signalling and no inflammatory response following an HFD. Conclusions/interpretation Findings from this study suggest that elevated mitochondrial ROS emission contributes to HFD-induced WAT insulin resistance.

show abstract

“…Quantitative real-time PCR RNA isolation and analysis was performed as previously described [25]. See the electronic supplementary material (ESM) for further details.…”

Section: Methodsmentioning

confidence: 99%

In adipose tissue, increased mitochondrial emission of reactive oxygen species is important for short-term high-fat diet-induced insulin resistance in mice

et al. 2015

Self Cite

View full text Add to dashboard Cite

show abstract

“…Recent results suggest mRNA stability decreases with muscle contraction or exercise in rodents (Lai et al 2010) along with increased mRNA-destabilizing proteins (Lai et al 2010;Matravadia et al 2013) and possibly with mRNA-stabilizing proteins (Lai et al 2010). In this regard, it has been suggested that mRNA destabilization is actually beneficial for accelerating adaptive responses in a subsequent bout of contraction (Lai et al 2010).…”

Section: Other Mechanisms Promoting Mitochondrial Biogenesismentioning

confidence: 99%

Molecular Basis of Exercise-Induced Skeletal Muscle Mitochondrial Biogenesis: Historical Advances, Current Knowledge, and Future Challenges

Perry

Hawley

2017

Cold Spring Harb Perspect Med

View full text Add to dashboard Cite

We provide an overview of groundbreaking studies that laid the foundation for our current understanding of exercise-induced mitochondrial biogenesis and its contribution to human skeletal muscle fitness. We highlight the mechanisms by which skeletal muscle responds to the acute perturbations in cellular energy homeostasis evoked by a single bout of endurancebased exercise and the adaptations resulting from the repeated demands of exercise training that ultimately promote mitochondrial biogenesis through hormetic feedback loops. Despite intense research efforts to elucidate the cellular mechanisms underpinning mitochondrial biogenesis in skeletal muscle, translating this basic knowledge into improved metabolic health at the population level remains a future challenge. E xercise represents a major challenge to multiple whole-body homeostatic functions. In an effort to overcome this challenge, numerous responses take place at the cellular and systemic levels that operate to blunt the homeostatic threats generated by exercise-induced increases in muscle energy turnover and oxygen demand . The capacity of skeletal muscle to adapt to repeated bouts of activity such that physical capacity is enhanced is termed exercise training. When considering endurance-based exercise (e.g., sustained activities that are .10 min duration and performed at 60% -90% of maximal oxygen uptake [VO 2max ] including sprint-interval training), the goals of such exercise are to induce an array of physiological and metabolic adaptations that enable an individual to increase the rate of energy production from both aerobic pathways, maintain tighter metabolic control (i.e., match adenosine triphosphate (ATP) production with ATP hydrolysis), minimize cellular perturbations, increase efficiency of motion, and improve the capacity of the trained musculature to resist

show abstract

“…Steady-state mRNA concentrations are the result of the balance between transcription and degradation. RNA-binding proteins (RBPs) that influence the stability of mRNA change in abundance and cellular location after contractile activity and can mediate the response to exercise (11,13). MicroRNA (miRNA) bind mRNA and regulate protein expression by impeding protein translation or causing mRNA degradation.…”

mentioning

confidence: 99%

The rigorous study of exercise adaptations: why mRNA might not be enough

Miller

Konopka

Hamilton

2016

Journal of Applied Physiology

View full text Add to dashboard Cite

show abstract

Exercise training increases the expression and nuclear localization of mRNA destabilizing proteins in skeletal muscle

Abstract: Matravadia S, Martino VB, Sinclair D, Mutch DM, Holloway GP. Exercise training increases the expression and nuclear localization of mRNA destabilizing proteins in skeletal muscle.

Cited by 9 publications

References 50 publications

In adipose tissue, increased mitochondrial emission of reactive oxygen species is important for short-term high-fat diet-induced insulin resistance in mice

In adipose tissue, increased mitochondrial emission of reactive oxygen species is important for short-term high-fat diet-induced insulin resistance in mice

Molecular Basis of Exercise-Induced Skeletal Muscle Mitochondrial Biogenesis: Historical Advances, Current Knowledge, and Future Challenges

The rigorous study of exercise adaptations: why mRNA might not be enough

Contact Info

Product

Resources

About