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Life (Basel, Switzerland)2021; 11(7); doi: 10.3390/life11070719

In Vitro Assays for the Assessment of Impaired Mitochondrial Bioenergetics in Equine Atypical Myopathy.

Abstract: Equine atypical myopathy is a seasonal intoxication of grazing equids. In Europe, this poisoning is associated with the ingestion of toxins contained in the seeds and seedlings of the sycamore maple (Acer pseudoplatanus). The toxins involved in atypical myopathy are known to inhibit ß-oxidation of fatty acids and induce a general decrease in mitochondrial respiration, as determined by high-resolution respirometry applied to muscle samples taken from cases of atypical myopathy. The severe impairment of mitochondrial bioenergetics induced by the toxins may explain the high rate of mortality observed: about 74% of horses with atypical myopathy die, most within the first two days of signs of poisoning. The mechanism of toxicity is not completely elucidated yet. To improve our understanding of the pathological process and to assess therapeutic candidates, we designed in vitro assays using equine skeletal myoblasts cultured from muscle biopsies and subjected to toxins involved in atypical myopathy. We established that equine primary myoblasts do respond to one of the toxins incriminated in the disease.
Publication Date: 2021-07-20 PubMed ID: 34357091PubMed Central: PMC8307747DOI: 10.3390/life11070719Google Scholar: Lookup
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  • Journal Article

Summary

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This research examines the impact of toxins associated with Equine Atypical Myopathy (a type of poisoning) on the efficiency of mitochondria in horse muscle cells. The study designs tests using cultured horse muscle cells exposed to these toxins.

Research Overview

Equine Atypical Myopathy (EAM) is a seasonally occurring intoxication found in grazing equids, primarily horses, and is particularly common in Europe. It’s associated with ingestion of toxins found in seeds and seedlings of the sycamore maple. The toxins related to EAM are known to disrupt the ß-oxidation of fatty acids, which is critical for energy production, thereby decreasing the efficiency of mitochondria – the powerhouses of cells. Using high-resolution respirometry on samples gathered from EAM cases, a significant decrease in mitochondrial respiration is observed. A mortality rate of about 74% is seen in horses with EAM, with most of them dying within the first two days of showing poisoning signs. However, the specific toxicity mechanism is not yet fully understood.

Methodology

  • The researchers aimed to enhance understanding of the pathological process and evaluate potential therapeutic measures.
  • The study designed in vitro assays (experiments conducted in controlled artificial environments), using equine skeletal myoblasts (precursor muscle cells) cultured from muscle biopsies and subjected to toxins associated with EAM. These tests were designed to mimic the in vivo (within the body) environment of EAM intoxication.

Findings

  • The researchers established that equine primary myoblasts do respond to one of the toxins implicated in EAM. This suggests the toxin has a direct impact on the precursor muscle cells, which might explain the high rate of muscle degradation observed in afflicted horses.
  • The research’s findings and in vitro experiments lay the groundwork for more detailed studies on horse muscle cell responses to various toxins, potentially enabling better understanding and treatment for EAM.

Cite This Article

APA
Kruse CJ, Stern D, Mouithys-Mickalad A, Niesten A, Art T, Lemieux H, Votion DM. (2021). In Vitro Assays for the Assessment of Impaired Mitochondrial Bioenergetics in Equine Atypical Myopathy. Life (Basel), 11(7). https://doi.org/10.3390/life11070719

Publication

ISSN: 2075-1729
NlmUniqueID: 101580444
Country: Switzerland
Language: English
Volume: 11
Issue: 7

Researcher Affiliations

Kruse, Caroline-J
  • Department of Functional Sciences, Faculty of Veterinary Medicine, Physiology and Sport Medicine, Fundamental and Applied Research for Animals & Health (FARAH), University of Liège, 4000 Liège, Belgium.
Stern, David
  • Equine Pole, Fundamental and Applied Research for Animals & Health (FARAH), Faculty of Veterinary Medicine, University of Liège, 4000 Liège, Belgium.
Mouithys-Mickalad, Ange
  • Center for Oxygen, Research & Development (CORD), Center for Interdisciplinary Research on Medicines (CIRM), Institute of Chemistry, B6a, University of Liège, Allée du Six Août, 11, 4000 Liège, Belgium.
Niesten, Ariane
  • Center for Oxygen, Research & Development (CORD), Fundamental and Applied Research for Animals & Health (FARAH), Institute of Chemistry, B6a, University of Liège, Allée du Six Août, 11, 4000 Liège, Belgium.
Art, Tatiana
  • Department of Functional Sciences, Faculty of Veterinary Medicine, Physiology and Sport Medicine, Fundamental and Applied Research for Animals & Health (FARAH), University of Liège, 4000 Liège, Belgium.
Lemieux, Hélène
  • Faculty Saint-Jean and Department of Medicine, University of Alberta, 8406-91 Street, Edmonton, AB T6C 4G9, Canada.
Votion, Dominique-M
  • Equine Pole, Fundamental and Applied Research for Animals & Health (FARAH), Faculty of Veterinary Medicine, University of Liège, 4000 Liège, Belgium.

Grant Funding

  • 40001860 / Fonds De La Recherche Scientifique - FNRS
  • R.CFRA.2991-J-F / Fonds spéciaux à la recherche, Université de Liège

Conflict of Interest Statement

The authors declare no conflict of interest.

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