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BDNF is a mediator of glycolytic fiber-type specification in mouse skeletal muscle
- Source :
- Proceedings of the National Academy of Sciences. 116:16111-16120
- Publication Year :
- 2019
- Publisher :
- Proceedings of the National Academy of Sciences, 2019.
-
Abstract
- Brain-derived neurotrophic factor (BDNF) influences the differentiation, plasticity, and survival of central neurons and likewise, affects the development of the neuromuscular system. Besides its neuronal origin, BDNF is also a member of the myokine family. However, the role of skeletal muscle-derived BDNF in regulating neuromuscular physiology in vivo remains unclear. Using gain- and loss-of-function animal models, we show that muscle-specific ablation of BDNF shifts the proportion of muscle fibers from type IIB to IIX, concomitant with elevated slow muscle-type gene expression. Furthermore, BDNF deletion reduces motor end plate volume without affecting neuromuscular junction (NMJ) integrity. These morphological changes are associated with slow muscle function and a greater resistance to contraction-induced fatigue. Conversely, BDNF overexpression promotes a fast muscle-type gene program and elevates glycolytic fiber number. These findings indicate that BDNF is required for fiber-type specification and provide insights into its potential modulation as a therapeutic target in muscle diseases.
- Subjects :
- 0301 basic medicine
Muscle Fibers, Skeletal
Biology
Models, Biological
Motor Endplate
Neuromuscular junction
03 medical and health sciences
0302 clinical medicine
Mediator
In vivo
Neurotrophic factors
Physical Conditioning, Animal
Myokine
Gene expression
medicine
Animals
Glycolysis
Gait
Mice, Knockout
Multidisciplinary
Brain-Derived Neurotrophic Factor
Skeletal muscle
Cell biology
030104 developmental biology
medicine.anatomical_structure
PNAS Plus
Gene Expression Regulation
nervous system
Organ Specificity
Muscle Fatigue
Oxidation-Reduction
Locomotion
030217 neurology & neurosurgery
Muscle Contraction
Signal Transduction
Subjects
Details
- ISSN :
- 10916490 and 00278424
- Volume :
- 116
- Database :
- OpenAIRE
- Journal :
- Proceedings of the National Academy of Sciences
- Accession number :
- edsair.doi.dedup.....ec080e6385cc13c9adb6eaf04a0f90f6