期刊
PLOS ONE
卷 8, 期 6, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0064525
关键词
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资金
- European Community's Health Seventh Framework Programme [259867]
- Thierry Latran Foundation
- Appel a Projets 2009 du Conseil Scientifique (University of Strasbourg)
- Association pour la Recherche sur la Sclerose Laterale Amyotrophique et autres Maladies du Motoneurone
- Higher Education Commission of the Pakistani government
- Association pour la Recherche et le Developpement de Moyens de Lutte contre les Maladies Neurodegeneratives (AREMANE)
- Association Francaise contre les Myopathies
- AREMANE
- FP7
- Chaire d'Exellence INSERM/Universite de Strasbourg
The progressive deterioration of the neuromuscular axis is typically observed in degenerative conditions of the lower motor neurons, such as amyotrophic lateral sclerosis (ALS). Neurodegeneration in this disease is associated with systemic metabolic perturbations, including hypermetabolism and dyslipidemia. Our previous gene profiling studies on ALS muscle revealed down-regulation of delta-9 desaturase, or SCD1, which is the rate-limiting enzyme in the synthesis of monounsaturated fatty acids. Interestingly, knocking out SCD1 gene is known to induce hypermetabolism and stimulate fatty acid beta-oxidation. Here we investigated whether SCD1 deficiency can affect muscle function and its restoration in response to injury. The genetic ablation of SCD1 was not detrimental per se to muscle function. On the contrary, muscles in SCD1 knockout mice shifted toward a more oxidative metabolism, and enhanced the expression of synaptic genes. Repressing SCD1 expression or reducing SCD-dependent enzymatic activity accelerated the recovery of muscle function after inducing sciatic nerve crush. Overall, these findings provide evidence for a new role of SCD1 in modulating the restorative potential of skeletal muscles.
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