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Bisphenol A enhances adipogenic signaling pathways in human mesenchymal stem cells
BACKGROUND: The endocrine disruptor Bisphenol-A (BPA), has been involved in dysregulating adipose tissue development and increasing the risk of obesity. The objective of this experiment was to investigate whether treatment of human mesenchymal stem cells with BPA could modulate adipogenesis and adip...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7065324/ https://www.ncbi.nlm.nih.gov/pubmed/32175033 http://dx.doi.org/10.1186/s41021-020-00150-6 |
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author | Salehpour, Amin Shidfar, Farzad Hedayati, Mehdi Neshatbini Tehrani, Asal Farshad, Ali Asghar Mohammadi, Saeed |
author_facet | Salehpour, Amin Shidfar, Farzad Hedayati, Mehdi Neshatbini Tehrani, Asal Farshad, Ali Asghar Mohammadi, Saeed |
author_sort | Salehpour, Amin |
collection | PubMed |
description | BACKGROUND: The endocrine disruptor Bisphenol-A (BPA), has been involved in dysregulating adipose tissue development and increasing the risk of obesity. The objective of this experiment was to investigate whether treatment of human mesenchymal stem cells with BPA could modulate adipogenesis and adipocyte differentiation. METHODS: In this experimental study, the human adipose-derived mesenchymal stem cells (hASCs) were cultured for 2 weeks with continuous exposure to 10(− 10) M or 10(− 8) M concentrations of BPA. The extent of triglyceride accumulation was visualized by Oil Red O staining. To evaluate BPA effect on the expression levels of key adipogenic trascripotion factors and proteins, we used Quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) and ELISA. RESULTS: The results presented a dose-dependent triglyceride accumulation in treated cells with BPA. Additionally, we observed that BPA induced transcription of the Peroxisome proliferator-activated receptor-gamma (PPARγ), CCAAT-enhancer-binding protein-alpha (C/EBPα), CCAAT-enhancer-binding protein-beta (C/EBPβ), sterol regulatory element-binding protein-1c (SREBP1c), Fatty acid synthase (FASN), and lipoprotein lipase (LPL); BPA suppressed the expression of Fatty acid binding protein-4 (FABP4) and Estrogen receptor-beta (ERβ). CONCLUSIONS: Our findings supported the hypothesis that BPA enhances adipogenic differentiation thereby may play a role in development of obesity and dysregulation of metabolic homoeostasis. |
format | Online Article Text |
id | pubmed-7065324 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-70653242020-03-13 Bisphenol A enhances adipogenic signaling pathways in human mesenchymal stem cells Salehpour, Amin Shidfar, Farzad Hedayati, Mehdi Neshatbini Tehrani, Asal Farshad, Ali Asghar Mohammadi, Saeed Genes Environ Research BACKGROUND: The endocrine disruptor Bisphenol-A (BPA), has been involved in dysregulating adipose tissue development and increasing the risk of obesity. The objective of this experiment was to investigate whether treatment of human mesenchymal stem cells with BPA could modulate adipogenesis and adipocyte differentiation. METHODS: In this experimental study, the human adipose-derived mesenchymal stem cells (hASCs) were cultured for 2 weeks with continuous exposure to 10(− 10) M or 10(− 8) M concentrations of BPA. The extent of triglyceride accumulation was visualized by Oil Red O staining. To evaluate BPA effect on the expression levels of key adipogenic trascripotion factors and proteins, we used Quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) and ELISA. RESULTS: The results presented a dose-dependent triglyceride accumulation in treated cells with BPA. Additionally, we observed that BPA induced transcription of the Peroxisome proliferator-activated receptor-gamma (PPARγ), CCAAT-enhancer-binding protein-alpha (C/EBPα), CCAAT-enhancer-binding protein-beta (C/EBPβ), sterol regulatory element-binding protein-1c (SREBP1c), Fatty acid synthase (FASN), and lipoprotein lipase (LPL); BPA suppressed the expression of Fatty acid binding protein-4 (FABP4) and Estrogen receptor-beta (ERβ). CONCLUSIONS: Our findings supported the hypothesis that BPA enhances adipogenic differentiation thereby may play a role in development of obesity and dysregulation of metabolic homoeostasis. BioMed Central 2020-03-11 /pmc/articles/PMC7065324/ /pubmed/32175033 http://dx.doi.org/10.1186/s41021-020-00150-6 Text en © The Author(s) 2020 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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. |
spellingShingle | Research Salehpour, Amin Shidfar, Farzad Hedayati, Mehdi Neshatbini Tehrani, Asal Farshad, Ali Asghar Mohammadi, Saeed Bisphenol A enhances adipogenic signaling pathways in human mesenchymal stem cells |
title | Bisphenol A enhances adipogenic signaling pathways in human mesenchymal stem cells |
title_full | Bisphenol A enhances adipogenic signaling pathways in human mesenchymal stem cells |
title_fullStr | Bisphenol A enhances adipogenic signaling pathways in human mesenchymal stem cells |
title_full_unstemmed | Bisphenol A enhances adipogenic signaling pathways in human mesenchymal stem cells |
title_short | Bisphenol A enhances adipogenic signaling pathways in human mesenchymal stem cells |
title_sort | bisphenol a enhances adipogenic signaling pathways in human mesenchymal stem cells |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7065324/ https://www.ncbi.nlm.nih.gov/pubmed/32175033 http://dx.doi.org/10.1186/s41021-020-00150-6 |
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