New insights into the skeletal muscle phenotype of equine motor neuron disease: a quantitative approach.
Abstract: Equine motor neuron disease (EMND) is a neurodegenerative disorder similar to the sporadic form of human amyotrophic lateral sclerosis. This study was conducted to quantify myofiber plasticity in response to EMND. Deep M. gluteus medius biopsy samples from eight horses with an ante mortem diagnosis of EMND, which in five cases was later confirmed by post mortem examination of spinal cord and peripheral nerves, were examined by combined methodologies of electrophoresis of myosin heavy chains (MyHC), muscle enzymes and substrate biochemistry, immunohistochemistry of MyHCs and sarcoendoplasmic Ca2+-ATPase (SERCA) isoforms, quantitative histochemistry of succinic dehydrogenase, glycerol-3-phosphate dehydrogenase, periodic acid-Schiff and capillaries, and photometric image analysis. The data were compared with muscle biopsies from healthy controls. Histopathological findings of EMND were observed in muscle biopsy specimens from all cases, but the severity and intra-biopsy extent varied from case to case. Compared with controls, muscle biopsy samples from EMND horses had a lower percentage of MyHC type I fibers, higher percentages of hybrid IIAX and pure IIX fibers, significant atrophy of all muscle fiber types, reduced oxidative capacity, increased glycolytic capacity, diminished intramuscular glycogen, lower capillary-to-fiber ratio, a higher ratio of myofibers expressing SERCA1a to SERCA2a isoforms, and a lower percentage of fibers expressing phospholamban. Objective discrimination of muscle biopsy specimens according to their healthy status (EMND vs controls) was possible on the basis of their muscular characteristics. A coordinated shift from slow to fast muscle characteristics in contractile and metabolic features of muscle fiber types, together with generalized myofiber atrophy, occurs in EMND and the extent of this change seems to be related to the duration of the disease.
Publication Date: 2004-12-22 PubMed ID: 15616793DOI: 10.1007/s00401-004-0940-1Google Scholar: Lookup
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- Comparative Study
- Journal Article
Summary
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The research article focuses on exploring the skeletal muscle phenotype composition in horses suffering from equine motor neuron disease (EMND) by conducting a quantitative study.
Background
- The study is centered around equine motor neuron disease (EMND), a neurodegenerative disorder in horses that has parallels with human amyotrophic lateral sclerosis (ALS). ALS is a disease that leads to the degeneration of motor neurons, decaying the muscles and leading to potential paralysis.
- The primary focus of this study is to quantify the plasticity or adaptability of myofiber (muscle fiber) in response to EMND.
Research Methodology
- Researchers studied muscle samples from eight horses diagnosed with EMND using varying methods including electrophoresis, muscle enzymes, and substrate biochemistry.
- Special attention was given to Myosin heavy chains (MyHC), elemental components of muscle fibers responsible for motility and contraction.
- Samples were also examined for Sarco/Endoplasmic Reticulum Calcium ATPase (SERCA) isoforms, essential proteins that facilitate muscular contraction and relaxation.
- The team used quantitative histochemistry techniques to study enzymes like succinic dehydrogenase and glycerol-3-phosphate dehydrogenase, and glycogen level amounts.
- The findings from EMND affected horses were contrasted with samples from healthy horses.
Observations and Outcomes
- All biopsy specimens from the EMND cases presented histopathological changes characteristic of the disease, though the severity and extent of these changes varied.
- Muscle samples from EMND horses showed a diminished percentage of type I fibers (slow-twitch, fatigue-resistant muscle fibers), and an increase in hybrid IIAX and pure IIX fibers (fast-twitch, fatigue-prone muscle fibers).
- The samples also showed significant muscle fiber atrophy, reduced oxidative capacity, increased glycolytic capacity, lower glycogen levels, and a reduced capillary-to-fiber ratio.
- A shift was observed in the balance of SERCA isoforms expressed in the muscle fibers. These findings suggest a coordinated shift from slow to fast muscle characteristics.
Conclusion
- The severeness of changes in muscle fiber types and a general atrophy of myofiber or muscle fibers is demonstrated in EMND, and the extent of this change seems to be linked to the progression time of the disease.
- The research outcomes provide the possibility of distinguishing between healthy and EMND affected horses based on their muscular properties.
Cite This Article
APA
Palencia P, Quiroz-Rothe E, Rivero JL.
(2004).
New insights into the skeletal muscle phenotype of equine motor neuron disease: a quantitative approach.
Acta Neuropathol, 109(3), 272-284.
https://doi.org/10.1007/s00401-004-0940-1 Publication
Researcher Affiliations
- Laboratory of Muscular Biopathology, Department of Comparative Anatomy and Pathological Anatomy, Faculty of Veterinary Science, University of Cordoba, Campus Universitario de Rabanales, Córdoba, Spain.
MeSH Terms
- Adenosine Triphosphatases / metabolism
- Animals
- Biopsy / methods
- Calcium-Binding Proteins / metabolism
- Calcium-Transporting ATPases / metabolism
- Citrate (si)-Synthase / metabolism
- Diagnostic Imaging / methods
- Electrophoresis, Polyacrylamide Gel / methods
- Female
- Glycogen / metabolism
- Histocytochemistry / methods
- Horse Diseases / metabolism
- Horse Diseases / pathology
- Horses
- Immunohistochemistry / methods
- L-Lactate Dehydrogenase / metabolism
- Male
- Motor Neuron Disease / metabolism
- Motor Neuron Disease / pathology
- Motor Neuron Disease / veterinary
- Muscle Fibers, Skeletal / classification
- Muscle Fibers, Skeletal / metabolism
- Muscle Fibers, Skeletal / pathology
- Muscle, Skeletal / metabolism
- Muscle, Skeletal / pathology
- Myosin Heavy Chains / metabolism
- Phenotype
- Principal Component Analysis / methods
- Protein Isoforms / metabolism
- Sarcoplasmic Reticulum Calcium-Transporting ATPases
- Succinate Dehydrogenase / metabolism
Citations
This article has been cited 5 times.- Arpke RW, Moritz TC, Hahn KL, Stark DA, Villalón E, Lorson CL, Cornelison D. Normal muscle fiber type distribution is recapitulated in aged ephrin-A3(-/-) mice that previously lacked most slow myofibers.. Am J Physiol Cell Physiol 2023 Mar 1;324(3):C718-C727.
- de Meeûs d'Argenteuil C, Boshuizen B, Vidal Moreno de Vega C, Leybaert L, de Maré L, Goethals K, De Spiegelaere W, Oosterlinck M, Delesalle C. Comparison of Shifts in Skeletal Muscle Plasticity Parameters in Horses in Three Different Muscles, in Answer to 8 Weeks of Harness Training.. Front Vet Sci 2021;8:718866.
- Díez de Castro E, Zafra R, Acevedo LM, Pérez J, Acosta I, Rivero JL, Aguilera-Tejero E. Eosinophilic Enteritis in Horses with Motor Neuron Disease.. J Vet Intern Med 2016 May;30(3):873-9.
- Liu W, Wei-LaPierre L, Klose A, Dirksen RT, Chakkalakal JV. Inducible depletion of adult skeletal muscle stem cells impairs the regeneration of neuromuscular junctions.. Elife 2015 Aug 27;4.
- Chin ER, Chen D, Bobyk KD, Mázala DA. Perturbations in intracellular Ca2+ handling in skeletal muscle in the G93A*SOD1 mouse model of amyotrophic lateral sclerosis.. Am J Physiol Cell Physiol 2014 Dec 1;307(11):C1031-8.
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