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Loss of miR-542-3p enhances IGFBP-1 expression in decidualizing human endometrial stromal cells
Endometrial decidualization represents an essential step for the successful implantation of the embryo; however, the molecular mechanism behind this differentiation process remains unclear. This study aimed to identify novel microRNAs (miRNAs) involved in the regulation of decidual gene expression i...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5209665/ https://www.ncbi.nlm.nih.gov/pubmed/28051155 http://dx.doi.org/10.1038/srep40001 |
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author | Tochigi, Hideno Kajihara, Takeshi Mizuno, Yosuke Mizuno, Yumi Tamaru, Shunsuke Kamei, Yoshimasa Okazaki, Yasushi Brosens, Jan J Ishihara, Osamu |
author_facet | Tochigi, Hideno Kajihara, Takeshi Mizuno, Yosuke Mizuno, Yumi Tamaru, Shunsuke Kamei, Yoshimasa Okazaki, Yasushi Brosens, Jan J Ishihara, Osamu |
author_sort | Tochigi, Hideno |
collection | PubMed |
description | Endometrial decidualization represents an essential step for the successful implantation of the embryo; however, the molecular mechanism behind this differentiation process remains unclear. This study aimed to identify novel microRNAs (miRNAs) involved in the regulation of decidual gene expression in human endometrial stromal cells (HESCs). An in vitro analysis of primary undifferentiated and decidualizing HESCs was conducted. HESCs were isolated from hysterectomy specimens from normally cycling premenopausal women with uterine fibroids, who were not on hormonal treatment at the time of surgery. Primary HESCs were expanded in culture and decidualized with 8-bromo-cyclic adenosine monophosphate and medroxyprogesterone acetate. Microarray analysis identified six miRNAs differentially expressed in response to decidualization of HESCs. All but one miRNA were downregulated upon decidualization, including miR-542-3p. We demonstrated that miR-542-3p overexpression inhibits the induction of major decidual marker genes, including IGFBP1, WNT4 and PRL. In addition, miR-542-3p overexpression inhibited the morphological transformation of HESCs in response to deciduogenic cues. A luciferase reporter assay confirmed that the 3′-untranslated region of IGFBP1 mRNA is targeted by miR-542-3p. The results suggest that miR-542-3p plays an important role in endometrial decidualization by regulating the expression of major decidual marker genes. |
format | Online Article Text |
id | pubmed-5209665 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-52096652017-01-04 Loss of miR-542-3p enhances IGFBP-1 expression in decidualizing human endometrial stromal cells Tochigi, Hideno Kajihara, Takeshi Mizuno, Yosuke Mizuno, Yumi Tamaru, Shunsuke Kamei, Yoshimasa Okazaki, Yasushi Brosens, Jan J Ishihara, Osamu Sci Rep Article Endometrial decidualization represents an essential step for the successful implantation of the embryo; however, the molecular mechanism behind this differentiation process remains unclear. This study aimed to identify novel microRNAs (miRNAs) involved in the regulation of decidual gene expression in human endometrial stromal cells (HESCs). An in vitro analysis of primary undifferentiated and decidualizing HESCs was conducted. HESCs were isolated from hysterectomy specimens from normally cycling premenopausal women with uterine fibroids, who were not on hormonal treatment at the time of surgery. Primary HESCs were expanded in culture and decidualized with 8-bromo-cyclic adenosine monophosphate and medroxyprogesterone acetate. Microarray analysis identified six miRNAs differentially expressed in response to decidualization of HESCs. All but one miRNA were downregulated upon decidualization, including miR-542-3p. We demonstrated that miR-542-3p overexpression inhibits the induction of major decidual marker genes, including IGFBP1, WNT4 and PRL. In addition, miR-542-3p overexpression inhibited the morphological transformation of HESCs in response to deciduogenic cues. A luciferase reporter assay confirmed that the 3′-untranslated region of IGFBP1 mRNA is targeted by miR-542-3p. The results suggest that miR-542-3p plays an important role in endometrial decidualization by regulating the expression of major decidual marker genes. Nature Publishing Group 2017-01-04 /pmc/articles/PMC5209665/ /pubmed/28051155 http://dx.doi.org/10.1038/srep40001 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Tochigi, Hideno Kajihara, Takeshi Mizuno, Yosuke Mizuno, Yumi Tamaru, Shunsuke Kamei, Yoshimasa Okazaki, Yasushi Brosens, Jan J Ishihara, Osamu Loss of miR-542-3p enhances IGFBP-1 expression in decidualizing human endometrial stromal cells |
title | Loss of miR-542-3p enhances IGFBP-1 expression in decidualizing human endometrial stromal cells |
title_full | Loss of miR-542-3p enhances IGFBP-1 expression in decidualizing human endometrial stromal cells |
title_fullStr | Loss of miR-542-3p enhances IGFBP-1 expression in decidualizing human endometrial stromal cells |
title_full_unstemmed | Loss of miR-542-3p enhances IGFBP-1 expression in decidualizing human endometrial stromal cells |
title_short | Loss of miR-542-3p enhances IGFBP-1 expression in decidualizing human endometrial stromal cells |
title_sort | loss of mir-542-3p enhances igfbp-1 expression in decidualizing human endometrial stromal cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5209665/ https://www.ncbi.nlm.nih.gov/pubmed/28051155 http://dx.doi.org/10.1038/srep40001 |
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