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Home / Equine Research Bank / Stem Cell Res Ther / MSI-1436 improves EMS adipose derived progenitor stem cells ...
Stem cell research & therapy2021; 12(1); 97; doi: 10.1186/s13287-020-02102-x

MSI-1436 improves EMS adipose derived progenitor stem cells in the course of adipogenic differentiation through modulation of ER stress, apoptosis, and oxidative stress.

Abstract: Protein tyrosine phosphatase 1B (PTP1B) is one of the major negative regulators of leptin and insulin signaling, and has been strongly implicated in insulin resistance development in the course of obesity and metabolic syndrome conditions; however, its exact role in controlling adipose tissue biogenesis is still poorly understood. This investigation aimed to elucidate whether selective inhibition of PTP1B using MSI-1436 compound may improve and restore the defective adipogenicity of ASCs isolated from EMS-affected horses. Equine ASC EMS cells were cultured under adipogenic conditions in the presence of PTP1B inhibitor and were subsequently tested for expression of the main adipogenic-related genes using RT-qPCR, changes in free fatty acid profiles by means of GC-MS technique, and for mitochondrial dynamics improvement through the analysis of mitochondrial transmembrane potential and oxidative stress. Selective inhibition of PTP1B in equine ASC EMS cells improved substantially adipogenic differentiation by promoting cellular proliferation and normalizing expression of C/EBPalpha, PPARγ, and Adipoq markers that are critical for proper adipogenesis. Levels of secreted adiponectin and PPARγ were also shown to be increased in MSI-1436-conditioned cells, while total leptin levels markedly dropped under the same conditions. Moreover, MSI-1436 treatment enabled the regulation of metabolic-related transcripts that are crosslink to adipogenesis, namely Akt1, Akt2, and SHBG. The obtained results demonstrated also an obvious reduction in intracellular accumulated ROS and NO, as well as mitigated ER stress through the downregulation of Chop, Perk, Atf6, Ire1, and Xbp1 transcripts upon PTP1B inhibition. Furthermore, general fluctuations in FFA composition of all differentiated groups have been highlighted, where palmitic acid, palmitoleic acid, stearic acid, and linolelaidic acid that are known to be associated with the development of metabolic disorders were found to be normalized upon PTP1B inhibition during adipogenic differentiation. The presented data provides the evidence that the use of PTP1B inhibitor may be successful in controlling and enhancing adipogenic differentiation of impaired equine ASCs affected by metabolic syndrome, and thus offers new insights for the management of obesity through the regulation of adipose tissue dynamics.
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Publication Date: 2021-02-03 PubMed ID: 33536069PubMed Central: PMC7860037DOI: 10.1186/s13287-020-02102-xGoogle 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.

The study explores the role of a specific protein, Protein tyrosine phosphatase 1B (PTP1B), in affecting adipose tissue growth in horses suffering from metabolic syndrome conditions. The use of a PTP1B inhibitor, MSI-1436, shows promising results in improving the growth and differentiation of adipose cells (adipogenesis).

Introduction

In this study, the researchers focus on the role of a protein called Protein tyrosine phosphatase 1B (PTP1B) which has been linked to negative regulation of insulin and leptin signaling in the body, contributing to insulin resistance and obesity. However, its specific role in the creation of adipose tissue (fat) is not fully understood. The researchers aim to see whether using MSI-1436, an inhibitor of PTP1B, can improve adipogenesis, especially in adipose stem cells (ASC) derived from horses suffering from equine metabolic syndrome (EMS).

Methods

The research team carried out experiments on equine ASC EMS cells by:

  • Culturing them under adipogenic conditions with the PTP1B inhibitor, MSI-1436
  • Testing these cells for expression of adipogenic-related genes
  • Checking changes in free fatty acid profiles using Gas Chromatography-Mass Spectrometry (GC-MS)
  • Analysing improvements in mitochondrial dynamics through looking at mitochondrial transmembrane potential and oxidative stress.

Results

The study showed that inhibition of PTP1B in equine ASC EMS cells greatly improved adipogenic differentiation.

  • The treatment promoted cellular proliferation and normalized the expression of critical adipogenic markers (C/EBPalpha, PPARγ, and AdipoQ).
  • There was an increase in the levels of secreted adiponectin and PPARγ, while leptin levels dropped.
  • Treatment also regulated metabolic-related transcripts linked to adipogenesis (Akt1, Akt2, and SHBG).
  • There was a significant reduction in accumulated reactive oxygen species (ROS) and nitric oxide (NO), along with a mitigation of ER stress through down-regulation of certain transcripts (Chop, Perk, Atf6, Ire1, and Xbp1).

Conclusions

Overall, the study provides evidence that PTP1B inhibition may be utilized to control and enhance adipogenic differentiation in impaired equine ASCs affected by metabolic syndrome. This could provide new strategic insights for managing obesity by regulating adipose tissue dynamics.

Cite This Article

APA
Bourebaba L, Kornicka-Garbowska K, Al Naem M, Röcken M, Łyczko J, Marycz K. (2021). MSI-1436 improves EMS adipose derived progenitor stem cells in the course of adipogenic differentiation through modulation of ER stress, apoptosis, and oxidative stress. Stem Cell Res Ther, 12(1), 97. https://doi.org/10.1186/s13287-020-02102-x

Publication

Stem cell research & therapy
ISSN: 1757-6512
NlmUniqueID: 101527581
Country: England
Language: English
Volume: 12
Issue: 1
Pages: 97
PII: 97

Researcher Affiliations

Bourebaba, Lynda
  • Department of Experimental Biology, Wrocław University of Environmental and Life Sciences, Norwida 27B Street, A7 Building, 50-375, Wrocław, Poland.
  • International Institute of Translational Medicine, Malin, Jesionowa 11, 55-114, Wisznia Mała, Poland.
Kornicka-Garbowska, Katarzyna
  • Department of Experimental Biology, Wrocław University of Environmental and Life Sciences, Norwida 27B Street, A7 Building, 50-375, Wrocław, Poland.
  • International Institute of Translational Medicine, Malin, Jesionowa 11, 55-114, Wisznia Mała, Poland.
Al Naem, Mohamad
  • Faculty of Veterinary Medicine, Equine Clinic-Equine Surgery, Justus-Liebig-University, 35392, Giessen, Germany.
Röcken, Michael
  • Faculty of Veterinary Medicine, Equine Clinic-Equine Surgery, Justus-Liebig-University, 35392, Giessen, Germany.
Łyczko, Jacek
  • Department of Chemistry, Faculty of Biotechnology and Food Science, Wrocław University of Environmental and Life Sciences, Norwida 25, 50-375, Wrocław, Poland.
Marycz, Krzysztof
  • Department of Experimental Biology, Wrocław University of Environmental and Life Sciences, Norwida 27B Street, A7 Building, 50-375, Wrocław, Poland. krzysztofmarycz@interia.pl.
  • International Institute of Translational Medicine, Malin, Jesionowa 11, 55-114, Wisznia Mała, Poland. krzysztofmarycz@interia.pl.
  • Faculty of Veterinary Medicine, Equine Clinic-Equine Surgery, Justus-Liebig-University, 35392, Giessen, Germany. krzysztofmarycz@interia.pl.

MeSH Terms

  • Adipogenesis
  • Adipose Tissue / metabolism
  • Animals
  • Apoptosis
  • Cell Differentiation
  • Cells, Cultured
  • Horses
  • Oxidative Stress
  • Stem Cells

Conflict of Interest Statement

The authors confirm that there are no conflicts of interest.

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