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MicroRNA-200c impairs uterine receptivity formation by targeting FUT4 and α1,3-fucosylation
Successful embryo implantation requires the establishment of a receptive endometrium. Poor endometrial receptivity has generally been considered as a major cause of infertility. Protein glycosylation is associated with many physiological and pathological processes. The fucosylation is catalyzed by t...
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/PMC5686352/ https://www.ncbi.nlm.nih.gov/pubmed/28914881 http://dx.doi.org/10.1038/cdd.2017.136 |
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author | Zheng, Qin Zhang, Dandan Yang, Y u Cui, Xinyuan Sun, Jiaqi Liang, Caixia Qin, Huamin Yang, Xuesong Liu, Shuai Yan, Qiu |
author_facet | Zheng, Qin Zhang, Dandan Yang, Y u Cui, Xinyuan Sun, Jiaqi Liang, Caixia Qin, Huamin Yang, Xuesong Liu, Shuai Yan, Qiu |
author_sort | Zheng, Qin |
collection | PubMed |
description | Successful embryo implantation requires the establishment of a receptive endometrium. Poor endometrial receptivity has generally been considered as a major cause of infertility. Protein glycosylation is associated with many physiological and pathological processes. The fucosylation is catalyzed by the specific fucosyltransferases. Fucosyltransferase IV (FUT4) is the key enzyme for the biosynthesis of α1,3-fucosylated glycans carried by glycoproteins, and the previous studies showed FUT4 expression changed dynamically during perimplantation. MicroRNAs (miRNAs) are known to regulate specific gene expression. However, the relationship between specific miRNA and FUT4, as well as the role of miRNA/FUT4 in the establishment of uterine receptivity remains elusive. In the current study, we reported that the levels of miR-200 family members were significantly increased in serum from infertility and abortion patients relative to healthy non-pregnancy and early-pregnancy women. Among these, miR-200c was the most sensitive diagnostic criterion for infertility by receiver operating characteristic curve analysis. FUT4 was lower in the serum from infertility and abortion patients compared with the healthy non-pregnancy and early-pregnancy women. Using endometrial cell lines and a mouse model, we demonstrated that miR-200c targeted and inhibited FUT4 expression, leading to the dysfunction of uterine receptivity. Our results also revealed that miR-200c decreased α1.3-fucosylation on glycoprotein CD44, which further inactivated Wnt/β-catenin signaling pathway. Taken together, miR-200c hampers uterine receptivity formation by targeting FUT4 and α1.3-fucosylation on CD44. miR-200c and FUT4 may be applied together as the potential markers for endometrial receptivity, and useful diagnostic and therapeutic targets for infertility. |
format | Online Article Text |
id | pubmed-5686352 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-56863522017-12-01 MicroRNA-200c impairs uterine receptivity formation by targeting FUT4 and α1,3-fucosylation Zheng, Qin Zhang, Dandan Yang, Y u Cui, Xinyuan Sun, Jiaqi Liang, Caixia Qin, Huamin Yang, Xuesong Liu, Shuai Yan, Qiu Cell Death Differ Original Paper Successful embryo implantation requires the establishment of a receptive endometrium. Poor endometrial receptivity has generally been considered as a major cause of infertility. Protein glycosylation is associated with many physiological and pathological processes. The fucosylation is catalyzed by the specific fucosyltransferases. Fucosyltransferase IV (FUT4) is the key enzyme for the biosynthesis of α1,3-fucosylated glycans carried by glycoproteins, and the previous studies showed FUT4 expression changed dynamically during perimplantation. MicroRNAs (miRNAs) are known to regulate specific gene expression. However, the relationship between specific miRNA and FUT4, as well as the role of miRNA/FUT4 in the establishment of uterine receptivity remains elusive. In the current study, we reported that the levels of miR-200 family members were significantly increased in serum from infertility and abortion patients relative to healthy non-pregnancy and early-pregnancy women. Among these, miR-200c was the most sensitive diagnostic criterion for infertility by receiver operating characteristic curve analysis. FUT4 was lower in the serum from infertility and abortion patients compared with the healthy non-pregnancy and early-pregnancy women. Using endometrial cell lines and a mouse model, we demonstrated that miR-200c targeted and inhibited FUT4 expression, leading to the dysfunction of uterine receptivity. Our results also revealed that miR-200c decreased α1.3-fucosylation on glycoprotein CD44, which further inactivated Wnt/β-catenin signaling pathway. Taken together, miR-200c hampers uterine receptivity formation by targeting FUT4 and α1.3-fucosylation on CD44. miR-200c and FUT4 may be applied together as the potential markers for endometrial receptivity, and useful diagnostic and therapeutic targets for infertility. Nature Publishing Group 2017-12 2017-09-15 /pmc/articles/PMC5686352/ /pubmed/28914881 http://dx.doi.org/10.1038/cdd.2017.136 Text en Copyright © 2017 The Author(s) http://creativecommons.org/licenses/by-nc-sa/4.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 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-nc-sa/4.0/ |
spellingShingle | Original Paper Zheng, Qin Zhang, Dandan Yang, Y u Cui, Xinyuan Sun, Jiaqi Liang, Caixia Qin, Huamin Yang, Xuesong Liu, Shuai Yan, Qiu MicroRNA-200c impairs uterine receptivity formation by targeting FUT4 and α1,3-fucosylation |
title | MicroRNA-200c impairs uterine receptivity formation by targeting FUT4 and α1,3-fucosylation |
title_full | MicroRNA-200c impairs uterine receptivity formation by targeting FUT4 and α1,3-fucosylation |
title_fullStr | MicroRNA-200c impairs uterine receptivity formation by targeting FUT4 and α1,3-fucosylation |
title_full_unstemmed | MicroRNA-200c impairs uterine receptivity formation by targeting FUT4 and α1,3-fucosylation |
title_short | MicroRNA-200c impairs uterine receptivity formation by targeting FUT4 and α1,3-fucosylation |
title_sort | microrna-200c impairs uterine receptivity formation by targeting fut4 and α1,3-fucosylation |
topic | Original Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5686352/ https://www.ncbi.nlm.nih.gov/pubmed/28914881 http://dx.doi.org/10.1038/cdd.2017.136 |
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