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Excessive Endoplasmic Reticulum Stress Correlates with Impaired Mitochondrial Dynamics, Mitophagy and Apoptosis, in Liver and Adipose Tissue, but Not in Muscles in EMS Horses

1
Department of Experimental Biology, Wroclaw University of Environmental and Life Sciences, 50-375 Wroclaw, Poland
2
Wroclaw Research Centre EIT+, ul. Stabłowicka 147, 54-066 Wrocław, Poland
3
PferdePraxis Dr. Med. Vet. Daniel Weiss, Postmatte 14, CH-8807 Freienbach, Switzerland
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2018, 19(1), 165; https://doi.org/10.3390/ijms19010165
Received: 18 December 2017 / Revised: 3 January 2018 / Accepted: 4 January 2018 / Published: 6 January 2018
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
Nowadays, endocrine disorders have become more frequent in both human and veterinary medicine. In horses, reduced physical activity combined with carbohydrate and sugar overload may result in the development of the so-called equine metabolic syndrome (EMS). EMS is characterized by insulin resistance, hyperinsulinemia, elevated blood triglyceride concentrations and usually obesity. Although the phenotypic features of EMS individuals are well known, the molecular mechanism underlying disease development remains elusive. Therefore, in the present study, we analyzed insulin-sensitive tissues, i.e., muscles, liver and adipose tissue in order to evaluate insulin resistance and apoptosis. Furthermore, we assessed mitochondrial dynamics and mitophagy in those tissues, because mitochondrial dysfunction is linked to the development of metabolic syndrome. We established the expression of genes related to insulin resistance, endoplasmic reticulum (ER) stress and mitochondria clearance by mitophagy using RT-PCR and Western blot. Cell ultrastructure was visualized using electron transmission microscopy. The results indicated that adipose tissue and liver of EMS horses were characterized by increased mitochondrial damage and mitophagy followed by triggering of apoptosis as mitophagy fails to restore cellular homeostasis. However, in muscles, apoptosis was reduced, suggesting the existence of a protective mechanism allowing that tissue to maintain homeostasis. View Full-Text
Keywords: metabolic syndrome; apoptosis; insulin resistance; mitochondria; autophagy metabolic syndrome; apoptosis; insulin resistance; mitochondria; autophagy
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Marycz, K.; Kornicka, K.; Szlapka-Kosarzewska, J.; Weiss, C. Excessive Endoplasmic Reticulum Stress Correlates with Impaired Mitochondrial Dynamics, Mitophagy and Apoptosis, in Liver and Adipose Tissue, but Not in Muscles in EMS Horses. Int. J. Mol. Sci. 2018, 19, 165.

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