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Hyunganol II Exerts Antiadipogenic Properties via MAPK-Mediated Suppression of PPARγ Expression in Human Bone Marrow-Derived Mesenchymal Stromal Cells
Bone marrow adiposity has been associated with several metabolic syndromes such as diabetes and osteoporosis. Imbalance in adipogenic and osteoblastogenic differentiation of human bone marrow mesenchymal stromal cells (hBM-MSCs) was suggested to be the cause of elevated bone marrow adiposity. There...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9592193/ https://www.ncbi.nlm.nih.gov/pubmed/36299776 http://dx.doi.org/10.1155/2022/4252917 |
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author | Oh, Jung Hwan Karadeniz, Fatih Seo, Youngwan Kong, Chang-Suk |
author_facet | Oh, Jung Hwan Karadeniz, Fatih Seo, Youngwan Kong, Chang-Suk |
author_sort | Oh, Jung Hwan |
collection | PubMed |
description | Bone marrow adiposity has been associated with several metabolic syndromes such as diabetes and osteoporosis. Imbalance in adipogenic and osteoblastogenic differentiation of human bone marrow mesenchymal stromal cells (hBM-MSCs) was suggested to be the cause of elevated bone marrow adiposity. There are several drugs, of both natural and synthetic origin, to treat bone loss. In this study, as a part of a recent trend to discover natural products with more biocompatibility and fewer side effects to treat bone loss, the effect of hyunganol II (HNG), a coumarin isolated from Corydalis heterocarpa, on hBM-MSC adipogenesis was investigated. Cells treated with HNG showed decreased lipid accumulation indicating a diminished adipocyte phenotype. Treatment with HNG also suppressed the mRNA and protein expressions of PPARγ, C/EBPα, and SREBP1c, and three adipogenic marker genes. Further analysis of MAPK signaling pathway exhibited that HNG treatment elevated ERK activation and suppressed the JNK-mediated cFos and cJun phosphorylation, which inhibits PPARγ transcriptional activity. Taken together, HNG treatment was shown to inhibit adipogenesis via suppressed PPARγ expression as a result of altered MAPK signaling. Therefore, it was suggested that HNG might prevent bone marrow adiposity by inhibiting hBM-MSC adipogenesis and can be utilized as a drug or nutraceutical with beneficial effects on bone. Thus, further studies should be conducted to analyze its effect in vivo. |
format | Online Article Text |
id | pubmed-9592193 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-95921932022-10-25 Hyunganol II Exerts Antiadipogenic Properties via MAPK-Mediated Suppression of PPARγ Expression in Human Bone Marrow-Derived Mesenchymal Stromal Cells Oh, Jung Hwan Karadeniz, Fatih Seo, Youngwan Kong, Chang-Suk Evid Based Complement Alternat Med Research Article Bone marrow adiposity has been associated with several metabolic syndromes such as diabetes and osteoporosis. Imbalance in adipogenic and osteoblastogenic differentiation of human bone marrow mesenchymal stromal cells (hBM-MSCs) was suggested to be the cause of elevated bone marrow adiposity. There are several drugs, of both natural and synthetic origin, to treat bone loss. In this study, as a part of a recent trend to discover natural products with more biocompatibility and fewer side effects to treat bone loss, the effect of hyunganol II (HNG), a coumarin isolated from Corydalis heterocarpa, on hBM-MSC adipogenesis was investigated. Cells treated with HNG showed decreased lipid accumulation indicating a diminished adipocyte phenotype. Treatment with HNG also suppressed the mRNA and protein expressions of PPARγ, C/EBPα, and SREBP1c, and three adipogenic marker genes. Further analysis of MAPK signaling pathway exhibited that HNG treatment elevated ERK activation and suppressed the JNK-mediated cFos and cJun phosphorylation, which inhibits PPARγ transcriptional activity. Taken together, HNG treatment was shown to inhibit adipogenesis via suppressed PPARγ expression as a result of altered MAPK signaling. Therefore, it was suggested that HNG might prevent bone marrow adiposity by inhibiting hBM-MSC adipogenesis and can be utilized as a drug or nutraceutical with beneficial effects on bone. Thus, further studies should be conducted to analyze its effect in vivo. Hindawi 2022-10-17 /pmc/articles/PMC9592193/ /pubmed/36299776 http://dx.doi.org/10.1155/2022/4252917 Text en Copyright © 2022 Jung Hwan Oh et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Oh, Jung Hwan Karadeniz, Fatih Seo, Youngwan Kong, Chang-Suk Hyunganol II Exerts Antiadipogenic Properties via MAPK-Mediated Suppression of PPARγ Expression in Human Bone Marrow-Derived Mesenchymal Stromal Cells |
title | Hyunganol II Exerts Antiadipogenic Properties via MAPK-Mediated Suppression of PPARγ Expression in Human Bone Marrow-Derived Mesenchymal Stromal Cells |
title_full | Hyunganol II Exerts Antiadipogenic Properties via MAPK-Mediated Suppression of PPARγ Expression in Human Bone Marrow-Derived Mesenchymal Stromal Cells |
title_fullStr | Hyunganol II Exerts Antiadipogenic Properties via MAPK-Mediated Suppression of PPARγ Expression in Human Bone Marrow-Derived Mesenchymal Stromal Cells |
title_full_unstemmed | Hyunganol II Exerts Antiadipogenic Properties via MAPK-Mediated Suppression of PPARγ Expression in Human Bone Marrow-Derived Mesenchymal Stromal Cells |
title_short | Hyunganol II Exerts Antiadipogenic Properties via MAPK-Mediated Suppression of PPARγ Expression in Human Bone Marrow-Derived Mesenchymal Stromal Cells |
title_sort | hyunganol ii exerts antiadipogenic properties via mapk-mediated suppression of pparγ expression in human bone marrow-derived mesenchymal stromal cells |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9592193/ https://www.ncbi.nlm.nih.gov/pubmed/36299776 http://dx.doi.org/10.1155/2022/4252917 |
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