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
Open Access
- 8 August 2016
- journal article
- research article
- Published by Hindawi Limited in Oxidative Medicine and Cellular Longevity
- Vol. 2016, 1-13
- https://doi.org/10.1155/2016/9047821
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.Keywords
Funding Information
- Association-Francaise Contre Les Myopathies (AFM 16670, 1161646, 1150589, 1161288, 3140396, P09-016-F, DI-741-15/N, 21161353, 21141242)
This publication has 54 references indexed in Scilit:
- Obesity Impairs Skeletal Muscle Regeneration Through Inhibition of AMPKDiabetes, 2015
- Angiotensin-(1–7) decreases skeletal muscle atrophy induced by angiotensin II through a Mas receptor-dependent mechanismClinical Science, 2014
- Expression of the Mas receptor is upregulated in skeletal muscle wastingHistochemistry and Cell Biology, 2014
- Enhanced trophic factor secretion by mesenchymal stem/stromal cells with Glycine-Histidine-Lysine (GHK)-modified alginate hydrogelsActa Biomaterialia, 2014
- Angiotensin II receptor type 1 blockade decreases CTGF/CCN2‐mediated damage and fibrosis in normal and dystrophic skeletal musclesJournal of Cellular and Molecular Medicine, 2011
- The role and regulation of MAFbx/atrogin-1 and MuRF1 in skeletal muscle atrophyPflügers Archiv - European Journal of Physiology, 2011
- Concise Review: Mesenchymal Stem/Multipotent Stromal Cells: The State of Transdifferentiation and Modes of Tissue Repair—Current ViewsThe International Journal of Cell Cloning, 2007
- Mesenchymal stem cells as trophic mediatorsJournal of Cellular Biochemistry, 2006
- TNF‐α acts via p38 MAPK to stimulate expression of the ubiquitin ligase atrogin1/MAFbx in skeletal muscleThe FASEB Journal, 2004
- TNF-α is involved in activating DNA fragmentation in skeletal muscleBritish Journal of Cancer, 2002