High Fat Diet-Induced Skeletal Muscle Wasting Is Decreased by Mesenchymal Stem Cells Administration: Implications on Oxidative Stress, Ubiquitin Proteasome Pathway Activation, and Myonuclear Apoptosis

Johanna Abrigo, Juan Carlos Rivera, Javier Aravena, Daniel Cabrera, Felipe Simon, Fernando Ezquer, Marcelo Ezquer, Claudio Cabello-Verrugio

Resultado de la investigación: Article

16 Citas (Scopus)

Resumen

Obesity can lead to skeletal muscle atrophy, a pathological condition characterized by the loss of strength and muscle mass. A feature of muscle atrophy is a decrease of myofibrillar proteins as a result of ubiquitin proteasome pathway overactivation, as evidenced by increased expression of the muscle-specific ubiquitin ligases atrogin-1 and MuRF-1. Additionally, other mechanisms are related to muscle wasting, including oxidative stress, myonuclear apoptosis, and autophagy. Stem cells are an emerging therapy in the treatment of chronic diseases such as high fat diet-induced obesity. Mesenchymal stem cells (MSCs) are a population of self-renewable and undifferentiated cells present in the bone marrow and other mesenchymal tissues of adult individuals. The present study is the first to analyze the effects of systemic MSC administration on high fat diet-induced skeletal muscle atrophy in the tibialis anterior of mice. Treatment with MSCs reduced losses of muscle strength and mass, decreases of fiber diameter and myosin heavy chain protein levels, and fiber type transitions. Underlying these antiatrophic effects, MSC administration also decreased ubiquitin proteasome pathway activation, oxidative stress, and myonuclear apoptosis. These results are the first to indicate that systemically administered MSCs could prevent muscle wasting associated with high fat diet-induced obesity and diabetes.

Idioma originalEnglish
Número de artículo9047821
PublicaciónOxidative Medicine and Cellular Longevity
Volumen2016
DOI
EstadoPublished - 1 ene 2016

Huella dactilar

Oxidative stress
High Fat Diet
Proteasome Endopeptidase Complex
Nutrition
Ubiquitin
Stem cells
Mesenchymal Stromal Cells
Muscle
Skeletal Muscle
Oxidative Stress
Chemical activation
Fats
Muscular Atrophy
Apoptosis
Obesity
Muscle Strength
Muscles
Myosin Heavy Chains
Autophagy
Ligases

ASJC Scopus subject areas

  • Biochemistry
  • Ageing
  • Cell Biology

Citar esto

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abstract = "Obesity can lead to skeletal muscle atrophy, a pathological condition characterized by the loss of strength and muscle mass. A feature of muscle atrophy is a decrease of myofibrillar proteins as a result of ubiquitin proteasome pathway overactivation, as evidenced by increased expression of the muscle-specific ubiquitin ligases atrogin-1 and MuRF-1. Additionally, other mechanisms are related to muscle wasting, including oxidative stress, myonuclear apoptosis, and autophagy. Stem cells are an emerging therapy in the treatment of chronic diseases such as high fat diet-induced obesity. Mesenchymal stem cells (MSCs) are a population of self-renewable and undifferentiated cells present in the bone marrow and other mesenchymal tissues of adult individuals. The present study is the first to analyze the effects of systemic MSC administration on high fat diet-induced skeletal muscle atrophy in the tibialis anterior of mice. Treatment with MSCs reduced losses of muscle strength and mass, decreases of fiber diameter and myosin heavy chain protein levels, and fiber type transitions. Underlying these antiatrophic effects, MSC administration also decreased ubiquitin proteasome pathway activation, oxidative stress, and myonuclear apoptosis. These results are the first to indicate that systemically administered MSCs could prevent muscle wasting associated with high fat diet-induced obesity and diabetes.",
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AU - Rivera, Juan Carlos

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AU - Simon, Felipe

AU - Ezquer, Fernando

AU - Ezquer, Marcelo

AU - Cabello-Verrugio, Claudio

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