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Experimental gerontology2017; 102; 19-27; doi: 10.1016/j.exger.2017.11.022

Skeletal muscle from aged American Quarter Horses shows impairments in mitochondrial biogenesis and expression of autophagy markers.

Abstract: Aging is associated with decreased mitochondrial content and function in skeletal muscle, possibly due to compromised biogenesis and autophagic removal of dysfunctional mitochondria. The aim of this study was to compare markers of mitochondrial content and biogenesis and of autophagy between skeletal muscle from young and aged American Quarter Horses. Citrate synthase protein and mtDNA copy number were decreased in triceps brachii (TB) muscle (P<0.05) from aged horses, suggesting an age-related decline in mitochondrial content. Concomitantly, mRNA expression of PGC-1α and TFAM, regulators of mitochondrial biogenesis, was lower in aged compared to young TB (P<0.05). Expression of autophagy markers suggested an age-associated decline of autophagy. The autophagosomal cargo protein SQSTM/p62 accumulated with age in both muscles (P<0.05). Expression of Autophagy-related protein Atg5 (P<0.05) and the autophagosome-bound form of Microtubule-associated protein light chain 3 (LC3-II; P<0.05) were lower in aged compared to young TB. While LC3 transcript level was elevated in aged compared to young GM (P<0.001), protein expression of LC3-II was unaffected. Gene expression of Lysosomal Membrane-Associated Protein 2 (LAMP2) was not affected by age in either muscle. However, LAMP2 protein expression declined with age (P<0.05), suggesting a decline in autophagosome-lysosome fusion. Taken together, our data indicate that equine skeletal muscle mitochondrial content and biogenesis were impaired with age. Further, autophagosome formation and lysosomal degradation were negatively affected in aged TB and GM, respectively. Future research needs to explore whether interventions targeting these cellular processes can prolong health and performance of aging American Quarter Horses.
Publication Date: 2017-12-02 PubMed ID: 29203401DOI: 10.1016/j.exger.2017.11.022Google Scholar: Lookup
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  • Journal Article

Summary

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This research investigates the impact of aging on the muscle health in American Quarter Horses. It found that as these horses age, their muscular strength declines due to decreased mitochondrial activity and less efficient removal of inefficient mitochondria.

Study Overview

  • The aim of this research was to investigate the effects of aging on skeletal muscular capacity in American Quarter Horses. The researchers specifically focused on the efficiency of mitochondrial creation and removal as the horses age.
  • The study measured the muscle protein content, number of mtDNA copies, expression of the genes TFAM and PGC-1α, which are regulators of mitochondrial creation, and the expression of autophagy or “self-eating” markers in both young and aged horses.

Key Findings

  • Markers of age-related mitochondrial decline, such as decreases in citrate synthase protein and mtDNA copy number, were observed in the triceps brachii, one of the major muscles in the horse. This suggested less mitochondrial content in aged horses.
  • Alongside this, the researchers found a decrease in mRNA expression of TFAM and PGC-1α in the same muscle group in older horses, indicating less mitochondrial biogenesis, or creation of new ones.
  • Moreover, the markers for autophagy, the process that removes older mitochondria to maintain cellular health, also showed a decline in aged horses. Particularly SQSTM/p62, a protein involved in autophagy, accumulated over time, and Atg5, another related protein, had less expression in older horses.
  • The researchers also found discrepancies in the LC3 gene and protein expression between the muscle groups of aged and young horses. While its gene expression level was higher in older horses, no change was detected in the protein level.
  • The expression of LAMP2, a protein responsible for fusing autophagosomes (structures that contain material to be degraded) with lysosomes (organelles responsible for degradation), remained the same on the gene level between young and aged horses, but the protein level saw a decline in the old horses.

Conclusion and Future Research

  • In conclusion, the researchers affirm that the capacity for mitochondrial content and biogenesis suffers with the aging of American Quarter Horses. Autophagosome formation and lysosomal degradation were also negatively affected with aging. This suggests that both the regeneration and removal of mitochondria in horse’s muscles are less efficient as they age.
  • The authors suggest that future research should be targeted at possible interventions to these cellular processes, with the hope of improving the health and performance of aging American Quarter Horses.

Cite This Article

APA
Li C, White SH, Warren LK, Wohlgemuth SE. (2017). Skeletal muscle from aged American Quarter Horses shows impairments in mitochondrial biogenesis and expression of autophagy markers. Exp Gerontol, 102, 19-27. https://doi.org/10.1016/j.exger.2017.11.022

Publication

ISSN: 1873-6815
NlmUniqueID: 0047061
Country: England
Language: English
Volume: 102
Pages: 19-27
PII: S0531-5565(17)30577-6

Researcher Affiliations

Li, Chengcheng
  • Department of Animal Sciences, University of Florida, Gainesville, FL, USA.
White, Sarah H
  • Department of Animal Sciences, University of Florida, Gainesville, FL, USA.
Warren, Lori K
  • Department of Animal Sciences, University of Florida, Gainesville, FL, USA.
Wohlgemuth, Stephanie E
  • Department of Animal Sciences, University of Florida, Gainesville, FL, USA. Electronic address: steffiw@ufl.edu.

MeSH Terms

  • Age Factors
  • Aging / genetics
  • Aging / metabolism
  • Aging / pathology
  • Animals
  • Autophagosomes / metabolism
  • Autophagosomes / pathology
  • Autophagy
  • Autophagy-Related Proteins / genetics
  • Autophagy-Related Proteins / metabolism
  • DNA, Mitochondrial / genetics
  • DNA, Mitochondrial / metabolism
  • Female
  • Gene Expression Regulation
  • Horses / genetics
  • Horses / metabolism
  • Lysosomes / metabolism
  • Lysosomes / pathology
  • Male
  • Mitochondria, Muscle / genetics
  • Mitochondria, Muscle / metabolism
  • Mitochondria, Muscle / pathology
  • Muscle, Skeletal / metabolism
  • Muscle, Skeletal / pathology
  • Organelle Biogenesis
  • Signal Transduction

Citations

This article has been cited 6 times.
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