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Tachtsis B, Smiles WJ, Lane SC, et al. Acute Endurance Exercise Induces Nuclear p53 Abundance in Human Skeletal Muscle. Front Physiol. 2016;7:144doi: 10.3389/fphys.2016.00144.
Tachtsis, B., Smiles, W. J., Lane, S. C., Hawley, J. A., & Camera, D. M. (2016). Acute Endurance Exercise Induces Nuclear p53 Abundance in Human Skeletal Muscle. Frontiers in physiology, 7144. https://doi.org/10.3389/fphys.2016.00144
Tachtsis, Bill, et al. "Acute Endurance Exercise Induces Nuclear p53 Abundance in Human Skeletal Muscle." Frontiers in physiology vol. 7 (2016): 144. doi: https://doi.org/10.3389/fphys.2016.00144
Tachtsis B, Smiles WJ, Lane SC, Hawley JA, Camera DM. Acute Endurance Exercise Induces Nuclear p53 Abundance in Human Skeletal Muscle. Front Physiol. 2016 Apr 26;7:144. doi: 10.3389/fphys.2016.00144. eCollection 2016. PMID: 27199762; PMCID: PMC4845512.
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Front Physiol. 2016 Apr 26;7:144. doi: 10.3389/fphys.2016.00144. eCollection 2016.

Acute Endurance Exercise Induces Nuclear p53 Abundance in Human Skeletal Muscle.

Frontiers in physiology

Bill Tachtsis, William J Smiles, Steven C Lane, John A Hawley, Donny M Camera

Affiliations

  1. Centre for Exercise and Nutrition, Mary MacKillop Institute for Health Research, Australian Catholic University Melbourne, VIC, Australia.
  2. Centre for Exercise and Nutrition, Mary MacKillop Institute for Health Research, Australian Catholic UniversityMelbourne, VIC, Australia; Research Institute for Sport and Exercise Sciences, Liverpool John Moores UniversityLiverpool, UK.
  3. Centre for Exercise and Nutrition, Mary MacKillop Institute for Health Research, Australian Catholic UniversityMelbourne, VIC, Australia; Exercise and Nutrition Research Group, School of Medical Sciences, RMIT UniversityMelbourne, VIC, Australia.

PMID: 27199762 PMCID: PMC4845512 DOI: 10.3389/fphys.2016.00144

Abstract

PURPOSE: The tumor suppressor protein p53 may have regulatory roles in exercise response-adaptation processes such as mitochondrial biogenesis and autophagy, although its cellular location largely governs its biological role. We investigated the subcellular localization of p53 and selected signaling targets in human skeletal muscle following a single bout of endurance exercise.

METHODS: Sixteen, untrained individuals were pair-matched for aerobic capacity (VO2peak) and allocated to either an exercise (EX, n = 8) or control (CON, n = 8) group. After a resting muscle biopsy, EX performed 60 min continuous cycling at ~70% of VO2peak during which time CON subjects rested. A further biopsy was obtained from both groups 3 h post-exercise (EX) or 4 h after the first biopsy (CON).

RESULTS: Nuclear p53 increased after 3 h recovery with EX only (~48%, p < 0.05) but was unchanged in the mitochondrial or cytoplasmic fractions in either group. Autophagy protein 5 (Atg-5) decreased in the mitochondrial protein fraction 3 h post-EX (~69%, P < 0.05) but remained unchanged in CON. There was an increase in cytoplasmic levels of the mitophagy marker PINK1 following 3 h of rest in CON only (~23%, P < 0.05). There were no changes in mitochondrial, nuclear, or cytoplasmic levels of PGC-1α post-exercise in either group.

CONCLUSIONS: The selective increase in nuclear p53 abundance following endurance exercise suggests a potential pro-autophagy response to remove damaged proteins and organelles prior to initiating mitochondrial biogenesis and remodeling responses in untrained individuals.

Keywords: autophagy; cell signaling; mitochondrial biogenesis; mitochondrial turnover; skeletal muscle

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