Inhibition of protein tyrosine phosphatase improves mitochondrial bioenergetics and dynamics, reduces oxidative stress, and enhances adipogenic differentiation potential in metabolically impaired progenitor stem cells

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Abstract

Background

Protein tyrosine phosphatase 1B (PTP1B) and low molecular weight protein tyrosine phosphatase (LMPTP) are implicated in the development of metabolic disorders. Yet, their role in progenitor stem cell adipogenic differentiation and modulation of mitochondrial dynamics remains elusive.

Methods

In this study, we decided to investigate whether inhibition of PTP1B and LMPTP enhance adipogenic differentiation of metabolically impaired progenitor stem cells via modulation of mitochondrial bioenergetics and dynamics. Cells were cultured under adipogenic conditions in the presence of PTP1B and LMPTP inhibitors, and were subjected to the analysis of the main adipogenic-related and mitochondrial-related genes using RT-qPCR. Protein levels were established with western blot while mitochondrial morphology with MicroP software.

Results

Selective inhibitors of both PTP1B and MPTP enhanced adipogenic differentiation of metabolically impaired progenitor stem cells. We have observed enhanced expression of PPARy and adiponectin in treated cells. What is more, increased antioxidative defence and alternations in mitochondrial bioenergetics were observed. We have found that inhibition of PTP1B as well as C23 activates oxidative phosphorylation and enhances mitochondrial fusion contributing to enhanced adipogenesis.

Conclusions

The presented data provides evidence that the application of PTP1B and LMPTP inhibitors enhances adipogenesis through the modulation of mitochondrial dynamics.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12964-021-00772-5.

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Most cited references 37

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The Global Epidemic of the Metabolic Syndrome

Mohammad G. Saklayen (2018)

Metabolic syndrome, variously known also as syndrome X, insulin resistance, etc., is defined by WHO as a pathologic condition characterized by abdominal obesity, insulin resistance, hypertension, and hyperlipidemia. Though there is some variation in the definition by other health care organization, the differences are minor. With the successful conquest of communicable infectious diseases in most of the world, this new non-communicable disease (NCD) has become the major health hazard of modern world. Though it started in the Western world, with the spread of the Western lifestyle across the globe, it has become now a truly global problem. The prevalence of the metabolic syndrome is often more in the urban population of some developing countries than in its Western counterparts. The two basic forces spreading this malady are the increase in consumption of high calorie-low fiber fast food and the decrease in physical activity due to mechanized transportations and sedentary form of leisure time activities. The syndrome feeds into the spread of the diseases like type 2 diabetes, coronary diseases, stroke, and other disabilities. The total cost of the malady including the cost of health care and loss of potential economic activity is in trillions. The present trend is not sustainable unless a magic cure is found (unlikely) or concerted global/governmental/societal efforts are made to change the lifestyle that is promoting it. There are certainly some elements in the causation of the metabolic syndrome that cannot be changed but many are amenable for corrections and curtailments. For example, better urban planning to encourage active lifestyle, subsidizing consumption of whole grains and possible taxing high calorie snacks, restricting media advertisement of unhealthy food, etc. Revitalizing old fashion healthier lifestyle, promoting old-fashioned foods using healthy herbs rather than oil and sugar, and educating people about choosing healthy/wholesome food over junks are among the steps that can be considered.

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Adipose Tissue Dysfunction as Determinant of Obesity-Associated Metabolic Complications

Michele Longo, Federica Zatterale, Jamal Naderi … (2019)

Obesity is a critical risk factor for the development of type 2 diabetes (T2D), and its prevalence is rising worldwide. White adipose tissue (WAT) has a crucial role in regulating systemic energy homeostasis. Adipose tissue expands by a combination of an increase in adipocyte size (hypertrophy) and number (hyperplasia). The recruitment and differentiation of adipose precursor cells in the subcutaneous adipose tissue (SAT), rather than merely inflating the cells, would be protective from the obesity-associated metabolic complications. In metabolically unhealthy obesity, the storage capacity of SAT, the largest WAT depot, is limited, and further caloric overload leads to the fat accumulation in ectopic tissues (e.g., liver, skeletal muscle, and heart) and in the visceral adipose depots, an event commonly defined as “lipotoxicity.” Excessive ectopic lipid accumulation leads to local inflammation and insulin resistance (IR). Indeed, overnutrition triggers uncontrolled inflammatory responses in WAT, leading to chronic low-grade inflammation, therefore fostering the progression of IR. This review summarizes the current knowledge on WAT dysfunction in obesity and its associated metabolic abnormalities, such as IR. A better understanding of the mechanisms regulating adipose tissue expansion in obesity is required for the development of future therapeutic approaches in obesity-associated metabolic complications.

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Targeting adipose tissue in the treatment of obesity-associated diabetes

Christine M Kusminski, Perry Bickel, Philipp Scherer (2016)

Adipose tissue regulates numerous physiological processes, and its dysfunction in obese humans is associated with disrupted metabolic homeostasis, insulin resistance and type 2 diabetes mellitus (T2DM). Although several US-approved treatments for obesity and T2DM exist, these are limited by adverse effects and a lack of effective long-term glucose control. In this Review, we provide an overview of the role of adipose tissue in metabolic homeostasis and assess emerging novel therapeutic strategies targeting adipose tissue, including adipokine-based strategies, promotion of white adipose tissue beiging as well as reduction of inflammation and fibrosis.

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Author and article information

Contributors

Katarzyna Kornicka-Garbowska:

ORCID: http://orcid.org/0000-0002-2311-5789

katarzyna.kornicka@gmail.com

Lynda Bourebaba: lynda06bourebaba@gmail.com

Michael Röcken: michael.roecken@vetmed.uni-giessen.de

Krzysztof Marycz: krzysztofmarycz@interia.pl

Journal

Journal ID (nlm-ta): Cell Commun Signal

Journal ID (iso-abbrev): Cell Commun Signal

Title: Cell Communication and Signaling : CCS

Publisher: BioMed Central (London )

ISSN (Electronic): 1478-811X

Publication date (Electronic): 3 November 2021

Publication date PMC-release: 3 November 2021

Publication date Collection: 2021

Volume: 19

Electronic Location Identifier: 106

Affiliations

[1 ]GRID grid.411200.6, ISNI 0000 0001 0694 6014, Department of Experimental Biology, , Wroclaw University of Environmental and Life Sciences, ; Norwida 27B Street, A7 building, 50-375 Wroclaw, Poland

[2 ]International Institute of Translational Medicine, Malin, Jesionowa 11, 55-114 Wisznia Mała, Poland

[3 ]GRID grid.8664.c, ISNI 0000 0001 2165 8627, Faculty of Veterinary Medicine, Equine Clinic-Equine Surgery, , Justus-Liebig University, ; 35392 Giessen, Germany

Author information

Katarzyna Kornicka-Garbowska http://orcid.org/0000-0002-2311-5789

Article

Publisher ID: 772

DOI: 10.1186/s12964-021-00772-5

PMC ID: 8565043

PubMed ID: 34732209

SO-VID: a6fd2dd2-9484-4f88-95c9-edddaa5b18e8

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 24 March 2021

Date accepted : 30 July 2021

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100004281, Narodowe Centrum Nauki;

Award ID: 2018/29/B/NZ7/02662

Award ID: 2017/27/N/NZ7/02343

Award Recipient : Katarzyna Kornicka-Garbowska Krzysztof Marycz

Custom metadata

ScienceOpen disciplines: Cell biology

Keywords: progenitor stem cells,adipogenesis,ptp1b,lmptp,mitochondria

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ScienceOpen disciplines: Cell biology

Keywords: progenitor stem cells, adipogenesis, ptp1b, lmptp, mitochondria

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Inhibition of protein tyrosine phosphatase improves mitochondrial bioenergetics and dynamics, reduces oxidative stress, and enhances adipogenic differentiation potential in metabolically impaired progenitor stem cells

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Abstract

Background

Methods

Results

Conclusions

Supplementary Information

Related collections

Stress signalling in stem cells

Most cited references 37

The Global Epidemic of the Metabolic Syndrome

Adipose Tissue Dysfunction as Determinant of Obesity-Associated Metabolic Complications

Targeting adipose tissue in the treatment of obesity-associated diabetes

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Cited by 7

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