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Home / Equine Research Bank / Int J Inflam / The PTP1B Inhibitor Trodusquemine (MSI-1436) Improves Glucos...
International journal of inflammation2023; 2023; 3803056; doi: 10.1155/2023/3803056

The PTP1B Inhibitor Trodusquemine (MSI-1436) Improves Glucose Uptake in Equine Metabolic Syndrome Affected Liver through Anti-Inflammatory and Antifibrotic Activity.

Abstract: Hyperactivation of protein tyrosine phosphatase (PTP1B) has been associated with several metabolic malfunctions ranging from insulin resistance, metaflammation, lipotoxicity, and hyperglycaemia. Liver metabolism failure has been proposed as a core element in underlying endocrine disorders through persistent inflammation and highly fibrotic phenotype. Unassigned: In this study, the outcomes of PTP1B inhibition using trodusquemine (MSI-1436) on key equine metabolic syndrome (EMS)-related alterations including inflammation, fibrosis, and glucose uptake have been analyzed in liver explants collected from EMS-affected horses using various analytical techniques, namely, flow cytometry, RT-qPCR, and Western blot. Unassigned: PTP1B inhibition using trodusquemine resulted in decreased proinflammatory cytokines (IL-1, TNF-, and IL-6) release from liver and PBMC affected by EMS and regulated expression of major proinflammatory microRNAs such as miR-802 and miR-211. Moreover, MSI-1436 enhanced the anti-inflammatory profile of livers by elevating the expression of IL-10 and IL-4 and activating CD4CD25Foxp3 regulatory T cells in treated PBMC. Similarly, the inhibitor attenuated fibrogenic pathways in the liver by downregulating TGF-/NOX1/4 axis and associated MMP-2/9 overactivation. Interestingly, PTP1B inhibition ameliorated the expression of TIMP-1 and Smad7, both important antifibrotic mediators. Furthermore, application of MSI-1436 was found to augment the abundance of glycosylated Glut-2, which subsequently expanded the glucose absorption in the EMS liver, probably due to an enhanced Glut-2 stability and half-life onto the plasma cell membranes. Unassigned: Taken together, the presented data suggest that the PTP1B inhibition strategy and the use of its specific inhibitor MSI-1436 represents a promising option for the improvement of liver tissue integrity and homeostasis in the course of EMS and adds more insights for ongoing clinical trials for human MetS management.
Copyright © 2023 Lynda Bourebaba et al.
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Publication Date: 2023-09-30 PubMed ID: 37808009PubMed Central: PMC10560121DOI: 10.1155/2023/3803056Google Scholar: Lookup
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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 research investigates the effects of trodusquemine (MSI-1436), an inhibitor of protein tyrosine phosphatase (PTP1B), on equine metabolic syndrome (EMS). The inhibitor was found to reduce inflammation and fibrosis while improving glucose absorption in the livers of EMS-affected horses.

Methodology of the Research

  • The study primarily involved testing the impacts of PTP1B inhibition using trodusquemine on crucial EMS-related alterations in liver explants from horses affected by EMS.
  • The research team used an array of analytical techniques, including flow cytometry, RT-qPCR, and Western blot.

Effects of PTP1B Inhibition on Proinflammatory Cytokines

  • The use of trodusquemine significantly reduced the release of proinflammatory cytokines—IL-1, TNF-, and IL-6—from the livers and PBMC of EMS-affected horses.
  • The inhibitor also regulated the expression of major proinflammatory microRNAs (miR-802 and miR-211), suggesting the potential to control inflammation in EMS cases.

Impacts on Anti-Inflammatory Profile and Fibrogenic Pathways

  • MSI-1436 elevated the presence of anti-inflammatory cytokines IL-10 and IL-4.
  • The treatment boosted the activation of CD4CD25Foxp3 regulatory T cells in treated PBMC, potentially enhancing anti-inflammatory responses.
  • Regarding fibrosis, MSI-1436 reduced the pathway by suppressing the TGF-/NOX1/4 axis and thus inhibiting overactivation of MMP-2/9. It also improved the expression of TIMP-1 and Smad7, integral mediators of antifibrotic processes.

Enhancement of Glucose Uptake

  • Significantly, the study found that the inhibitor increased the amount of glycosylated Glut-2, leading to an improved glucose absorption capacity in the EMS-affected liver.
  • It is proposed that this might be due to an enhanced Glut-2 stability and half-life on plasma cell membranes.

Concluding Implications of the Study

  • The data suggests that employing a strategy of PTP1B inhibition, coupled with the use of its specific inhibitor MSI-1436, could be beneficial in improving liver tissue stability and overall operation in EMS.
  • These findings contribute valuable knowledge toward ongoing clinical trials focused on improving management of metabolic syndrome (MetS) in humans.

Cite This Article

APA
Bourebaba L, Serwotka-Suszczak A, Bourebaba N, Zyzak M, Marycz K. (2023). The PTP1B Inhibitor Trodusquemine (MSI-1436) Improves Glucose Uptake in Equine Metabolic Syndrome Affected Liver through Anti-Inflammatory and Antifibrotic Activity. Int J Inflam, 2023, 3803056. https://doi.org/10.1155/2023/3803056

Publication

International journal of inflammation
ISSN: 2090-8040
NlmUniqueID: 101538188
Country: United States
Language: English
Volume: 2023
Pages: 3803056
PII: 3803056

Researcher Affiliations

Bourebaba, Lynda
  • Department of Experimental Biology, Faculty of Biology and Animal Science, Wrocław University of Environmental and Life Sciences, Norwida 27B, Wrocław 50-375, Poland.
Serwotka-Suszczak, Anna
  • Department of Experimental Biology, Faculty of Biology and Animal Science, Wrocław University of Environmental and Life Sciences, Norwida 27B, Wrocław 50-375, Poland.
Bourebaba, Nabila
  • Department of Experimental Biology, Faculty of Biology and Animal Science, Wrocław University of Environmental and Life Sciences, Norwida 27B, Wrocław 50-375, Poland.
Zyzak, Magdalena
  • Department of Experimental Biology, Faculty of Biology and Animal Science, Wrocław University of Environmental and Life Sciences, Norwida 27B, Wrocław 50-375, Poland.
Marycz, Krzysztof
  • Department of Experimental Biology, Faculty of Biology and Animal Science, Wrocław University of Environmental and Life Sciences, Norwida 27B, Wrocław 50-375, Poland.
  • Department of Veterinary Medicine and Epidemiology, Veterinary Institute for Regenerative Cures, School of Veterinary Medicine, University of California, Davis, CA 95516, USA.

Conflict of Interest Statement

The authors declare that they have no conflicts of interest.

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