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Evaluation of Injury-induced Senescence and In Vivo Reprogramming in the Skeletal Muscle
Published on: October 26, 2017
Tubular aggregates in the skeletal muscle of the senescence-accelerated mouse; SAM
T Nishikawa1, J A Takahashi, T Matsushita
1Department of Neurosurgery, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto, Japan.
Abstract:
We investigated the skeletal muscles of nine strains of senescence accelerated mouse (SAM), DDD, AKR/J, C57BL/6J, A/J and BALB/c mice. We found that male SAMP8, SAMP7, C57BL/6J, A/J and BALB/c mice expressed tubular aggregates (TAs) in their skeletal muscle. Among these strains, the SAMP8 strain, which exhibits a short life span and various age-associated neurodegenerative disorders plus mitochondrial dysfunction, showed TAs more markedly than the others. Thus, we compared SAMP8 mice against SAMR1 mice, an accelerated senescence-resistant strain. Light- and electron micrographs showed that male SAMP8 mice exhibited an age-dependent aggravation of TA accumulation. There were no significant differences in the serum lactate/pyruvate levels between the SAMP8 and SAMR1 mice. However, the serum creatine kinase (CK) levels of the 3 and 6-month-old SAMP8 mice were higher than that of the corresponding SAMR1 mice. Considering the serum CK levels and the mitochondrial dysfunction of SAMP8 mice, we conclude that the TAs may be involved in the homeostasis of energy metabolism that is not appropriately regulated in the SAMP8 mouse mitochondrion.
Insights
Senescence accelerated mice (SAM) models, particularly SAMP8, show increased tubular aggregates (TAs) in skeletal muscle, linked to energy metabolism and mitochondrial dysfunction.
Area of Science:
- Gerontology
- Mitochondrial Biology
- Skeletal Muscle Physiology
Background:
- Senescence accelerated mouse (SAM) models are crucial for studying aging.
- Tubular aggregates (TAs) are observed in skeletal muscle, but their role in aging is not fully understood.
- SAMP8 mice exhibit premature aging, neurodegeneration, and mitochondrial dysfunction.
Purpose of the Study:
- To investigate the presence and accumulation of tubular aggregates (TAs) in the skeletal muscle of various mouse strains, with a focus on senescence-accelerated models.
- To compare TA accumulation in SAMP8 mice with a senescence-resistant strain (SAMR1) to understand age-related changes.
- To explore the potential link between TA accumulation, mitochondrial dysfunction, and energy metabolism in aging mice.
Main Methods:
- Comparative analysis of skeletal muscle from nine mouse strains, including senescence-accelerated (SAM) and control strains.
- Histological examination using light and electron microscopy to identify and quantify tubular aggregates (TAs).
- Biochemical analysis of serum markers, including lactate/pyruvate and creatine kinase (CK) levels, in SAMP8 and SAMR1 mice.
Main Results:
- Male mice from SAMP8, SAMP7, C57BL/6J, A/J, and BALB/c strains exhibited TAs in skeletal muscle.
- SAMP8 mice showed markedly higher TA accumulation compared to other strains, with age-dependent aggravation.
- Elevated serum CK levels were observed in 3 and 6-month-old SAMP8 mice compared to SAMR1 mice, despite similar lactate/pyruvate levels.
Conclusions:
- Tubular aggregates (TAs) are prevalent in the skeletal muscle of specific aging mouse strains, notably SAMP8.
- TA accumulation in SAMP8 mice is age-dependent and associated with elevated serum CK levels.
- TAs may play a role in the dysregulated energy metabolism and mitochondrial dysfunction observed in the SAMP8 mouse model of accelerated aging.
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