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Resveratrol promotes trophoblast invasion in pre‐eclampsia by inducing epithelial‐mesenchymal transition
Impairment spiral arteries remodelling was considered to be the underlying cause of pathogenesis of pre‐eclampsia (PE). Resveratrol (RE) was reported that it could modulate cellar phenotype to ameliorate diverse human diseases. However, the biological function of RE in PE remains poorly understood....
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6433653/ https://www.ncbi.nlm.nih.gov/pubmed/30710417 http://dx.doi.org/10.1111/jcmm.14175 |
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author | Zou, Yanfen Li, Shuhong Wu, Dan Xu, Yetao Wang, Sailan Jiang, Ying Liu, Fang Jiang, Ziyan Qu, Hongmei Yu, Xiang Wang, Xiaoli Wang, Yuanli Sun, Lizhou |
author_facet | Zou, Yanfen Li, Shuhong Wu, Dan Xu, Yetao Wang, Sailan Jiang, Ying Liu, Fang Jiang, Ziyan Qu, Hongmei Yu, Xiang Wang, Xiaoli Wang, Yuanli Sun, Lizhou |
author_sort | Zou, Yanfen |
collection | PubMed |
description | Impairment spiral arteries remodelling was considered to be the underlying cause of pathogenesis of pre‐eclampsia (PE). Resveratrol (RE) was reported that it could modulate cellar phenotype to ameliorate diverse human diseases. However, the biological function of RE in PE remains poorly understood. In this report, we investigated the effect of RE on trophoblast phenotype both in vivo and in vitro. We conducted MTT and transwell assays to explore cell proliferation and invasion events in HTR‐8/SVneo. In mice model, the clinical characteristics of PE were established through the injection of NG‐nitro‐l‐arginine methyl ester (L‐NAME). Furthermore, related experiments were performed to detect cellar phenotype‐associated signalling pathway, including epithelial‐mesenchymal transition (EMT) and Wnt/β‐catenin. Cell assays indicated that RE could increase trophoblasts migration and invasion. In addition, hypertension and proteinuria were markedly ameliorated by RE compared with the controls in PE mice model. Moreover, treatment by RE in trophoblasts or in PE model, we found that RE activated EMT progress through the regulation of E‐cadherin, β‐catenin, N‐cadherin, vimentin expression, and further altered the WNT‐related gene expression, including WNT1, WNT3 and WNT5B. Our findings demonstrated that RE might stimulate the invasive capability of human trophoblasts by promoting EMT and mediating the Wnt/β‐catenin pathway in PE. |
format | Online Article Text |
id | pubmed-6433653 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-64336532019-04-08 Resveratrol promotes trophoblast invasion in pre‐eclampsia by inducing epithelial‐mesenchymal transition Zou, Yanfen Li, Shuhong Wu, Dan Xu, Yetao Wang, Sailan Jiang, Ying Liu, Fang Jiang, Ziyan Qu, Hongmei Yu, Xiang Wang, Xiaoli Wang, Yuanli Sun, Lizhou J Cell Mol Med Original Articles Impairment spiral arteries remodelling was considered to be the underlying cause of pathogenesis of pre‐eclampsia (PE). Resveratrol (RE) was reported that it could modulate cellar phenotype to ameliorate diverse human diseases. However, the biological function of RE in PE remains poorly understood. In this report, we investigated the effect of RE on trophoblast phenotype both in vivo and in vitro. We conducted MTT and transwell assays to explore cell proliferation and invasion events in HTR‐8/SVneo. In mice model, the clinical characteristics of PE were established through the injection of NG‐nitro‐l‐arginine methyl ester (L‐NAME). Furthermore, related experiments were performed to detect cellar phenotype‐associated signalling pathway, including epithelial‐mesenchymal transition (EMT) and Wnt/β‐catenin. Cell assays indicated that RE could increase trophoblasts migration and invasion. In addition, hypertension and proteinuria were markedly ameliorated by RE compared with the controls in PE mice model. Moreover, treatment by RE in trophoblasts or in PE model, we found that RE activated EMT progress through the regulation of E‐cadherin, β‐catenin, N‐cadherin, vimentin expression, and further altered the WNT‐related gene expression, including WNT1, WNT3 and WNT5B. Our findings demonstrated that RE might stimulate the invasive capability of human trophoblasts by promoting EMT and mediating the Wnt/β‐catenin pathway in PE. John Wiley and Sons Inc. 2019-02-01 2019-04 /pmc/articles/PMC6433653/ /pubmed/30710417 http://dx.doi.org/10.1111/jcmm.14175 Text en © 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Zou, Yanfen Li, Shuhong Wu, Dan Xu, Yetao Wang, Sailan Jiang, Ying Liu, Fang Jiang, Ziyan Qu, Hongmei Yu, Xiang Wang, Xiaoli Wang, Yuanli Sun, Lizhou Resveratrol promotes trophoblast invasion in pre‐eclampsia by inducing epithelial‐mesenchymal transition |
title | Resveratrol promotes trophoblast invasion in pre‐eclampsia by inducing epithelial‐mesenchymal transition |
title_full | Resveratrol promotes trophoblast invasion in pre‐eclampsia by inducing epithelial‐mesenchymal transition |
title_fullStr | Resveratrol promotes trophoblast invasion in pre‐eclampsia by inducing epithelial‐mesenchymal transition |
title_full_unstemmed | Resveratrol promotes trophoblast invasion in pre‐eclampsia by inducing epithelial‐mesenchymal transition |
title_short | Resveratrol promotes trophoblast invasion in pre‐eclampsia by inducing epithelial‐mesenchymal transition |
title_sort | resveratrol promotes trophoblast invasion in pre‐eclampsia by inducing epithelial‐mesenchymal transition |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6433653/ https://www.ncbi.nlm.nih.gov/pubmed/30710417 http://dx.doi.org/10.1111/jcmm.14175 |
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