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Home / Equine Research Bank / Cells / Obesity Affects the Proliferative Potential of Equine Endome...
Cells2022; 11(9); 1437; doi: 10.3390/cells11091437

Obesity Affects the Proliferative Potential of Equine Endometrial Progenitor Cells and Modulates Their Molecular Phenotype Associated with Mitochondrial Metabolism.

Abstract: The study aimed to investigate the influence of obesity on cellular features of equine endometrial progenitor cells (Eca EPCs), including viability, proliferation capacity, mitochondrial metabolism, and oxidative homeostasis. Eca EPCs derived from non-obese (non-OB) and obese (OB) mares were characterized by cellular phenotype and multipotency. Obesity-induced changes in the activity of Eca EPCs include the decline of their proliferative activity, clonogenic potential, mitochondrial metabolism, and enhanced oxidative stress. Eca EPCs isolated from obese mares were characterized by an increased occurrence of early apoptosis, loss of mitochondrial dynamics, and senescence-associated phenotype. Attenuated metabolism of Eca EPCs OB was related to increased expression of pro-apoptotic markers (CASP9, BAX, P53, P21), enhanced expression of OPN, PI3K, and AKT, simultaneously with decreased signaling stabilizing cellular homeostasis (including mitofusin, SIRT1, FOXP3). Obesity alters functional features and the self-renewal potential of endometrial progenitor cells. The impaired cytophysiology of progenitor cells from obese endometrium predicts lower regenerative capacity if used as autologous transplants.
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Publication Date: 2022-04-24 PubMed ID: 35563743PubMed Central: PMC9100746DOI: 10.3390/cells11091437Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

This research focuses on studying how obesity influences the cellular traits of horse-derived endometrial cells including their survival, proliferation capabilities, cellular energy metabolism, and maintenance of a balanced internal state. The study suggests that obesity in horses can induce several changes in these cells, some of which include a decrease in their proliferation activity, potential for cloning, energy metabolism, an increase in oxidative stress, and early onset of apoptosis.

Research Objective and Methodology

  • The main purpose of this study was to understand how obesity affects the cellular characteristics of equine endometrial progenitor cells(Eca EPCs), and also their viability, reproduction capacity, mitochondrial activities, and their ability to maintain an equilibrium internal state, also known as oxidative homeostasis depending on the mare’s weight (obese or non-obese).
  • The Eca EPCs were sourced from both non-obese (non-OB) and obese (OB) horses, and their cellular traits and multipotency were examined.

Findings and Implications

  • The findings indicated that obesity induced several changes in how the progenitor cells behaved. The changes included a significant decrease in cell multiplication, ability to grow into colonies, their mitochondrial activities, and an increase in oxidative stress.
  • The Eca EPCs from obese mares showed an increased instance of early apoptosis, loss of mitochondrial dynamics, and a phenotype associated with cellular senescence, or ageing.
  • A slowing metabolism in Eca EPCs from obese mares was seen to be related to an increased expression of pro-apoptotic markers such as CASP9, BAX, P53, P21, an enhanced expression of OPN, PI3K, and AKT; all while experiencing a reduction in the signalling stabilizing cellular homeostasis (including mitofusin, SIRT1, FOXP3).
  • Therefore, obesity was found to alter functional aspects and the self-rejuvenation potential of these endometrial progenitor cells.
  • Furthermore, the impaired physiology of the progenitor cells from an obese endometrium suggests that their regenerative capacity would be diminished if used as self-donated transplants.

Cite This Article

APA
Smieszek A, Marcinkowska K, Pielok A, Sikora M, Valihrach L, Carnevale E, Marycz K. (2022). Obesity Affects the Proliferative Potential of Equine Endometrial Progenitor Cells and Modulates Their Molecular Phenotype Associated with Mitochondrial Metabolism. Cells, 11(9), 1437. https://doi.org/10.3390/cells11091437

Publication

Cells
ISSN: 2073-4409
NlmUniqueID: 101600052
Country: Switzerland
Language: English
Volume: 11
Issue: 9
PII: 1437

Researcher Affiliations

Smieszek, Agnieszka
  • Department of Experimental Biology, Faculty of Biology and Animal Science, University of Environmental and Life Sciences, Norwida 27B St., 50-375 Wroclaw, Poland.
Marcinkowska, Klaudia
  • Department of Experimental Biology, Faculty of Biology and Animal Science, University of Environmental and Life Sciences, Norwida 27B St., 50-375 Wroclaw, Poland.
Pielok, Ariadna
  • Department of Experimental Biology, Faculty of Biology and Animal Science, University of Environmental and Life Sciences, Norwida 27B St., 50-375 Wroclaw, Poland.
Sikora, Mateusz
  • Department of Experimental Biology, Faculty of Biology and Animal Science, University of Environmental and Life Sciences, Norwida 27B St., 50-375 Wroclaw, Poland.
Valihrach, Lukas
  • Laboratory of Gene Expression, Institute of Biotechnology CAS, Biocev, 25250 Vestec, Czech Republic.
Carnevale, Elaine
  • Equine Reproduction Laboratory, Department of Biomedical Sciences, Colorado State University, Fort Colins, CO 80523-1693, USA.
Marycz, Krzysztof
  • Department of Experimental Biology, Faculty of Biology and Animal Science, University of Environmental and Life Sciences, Norwida 27B St., 50-375 Wroclaw, Poland.
  • International Institute of Translational Medicine, Jesionowa 11 St., 55-124 Malin, Poland.

MeSH Terms

  • Animals
  • Endometrium / metabolism
  • Endothelial Progenitor Cells / metabolism
  • Female
  • Horses
  • Obesity / metabolism
  • Phenotype
  • Stem Cells / metabolism

Conflict of Interest Statement

The authors declare no conflict of interest.

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