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Elevated microRNA-125b inhibits cytotrophoblast invasion and impairs endothelial cell function in preeclampsia

Preeclampsia (PE) is a life-threatening disorder of human pregnancy affecting 5–8% of all pregnancies. Currently, PE remains an elusive complicated and heterogenous medical condition with no early marker or symptoms is recognized for this serious pregnancy complications. Here, we profiled the plasma...

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Autores principales: Li, Qinghua, Han, Yangyang, Xu, Peng, Yin, Lingxuan, Si, Yanru, Zhang, Cuijuan, Meng, Yuhan, Feng, Weiguo, Pan, Zhifang, Gao, Zhiqin, Li, Jie, Yang, Weiwei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7220944/
https://www.ncbi.nlm.nih.gov/pubmed/32435510
http://dx.doi.org/10.1038/s41420-020-0269-0
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author Li, Qinghua
Han, Yangyang
Xu, Peng
Yin, Lingxuan
Si, Yanru
Zhang, Cuijuan
Meng, Yuhan
Feng, Weiguo
Pan, Zhifang
Gao, Zhiqin
Li, Jie
Yang, Weiwei
author_facet Li, Qinghua
Han, Yangyang
Xu, Peng
Yin, Lingxuan
Si, Yanru
Zhang, Cuijuan
Meng, Yuhan
Feng, Weiguo
Pan, Zhifang
Gao, Zhiqin
Li, Jie
Yang, Weiwei
author_sort Li, Qinghua
collection PubMed
description Preeclampsia (PE) is a life-threatening disorder of human pregnancy affecting 5–8% of all pregnancies. Currently, PE remains an elusive complicated and heterogenous medical condition with no early marker or symptoms is recognized for this serious pregnancy complications. Here, we profiled the plasma miRNA expression patterns associated with preeclampsia and found 16 miRNAs were deregulated (p < 0.01) in patients who later developed PE. Circulating hsa-miR-125b was aberrantly upregulated in early pregnancy and significantly reduced after delivery in preeclampsia. We then investigated the underlying molecular mechanisms between miR-125b and PE in vitro. We found that upregulated miR-125b can target KCNA1 to inhibit trophoblast invasion in human trophoblast cells. Moreover, overexpression of miR-125b in HUVECs impaired endothelial cell function through GPC1. The findings indicated that upregulated miR-125b leads to impaired placentation, and an increased risk of preeclampsia, Our studies provide novel insights into the underlying mechanisms on the association of miR-125b in early pregnancy and risk of PE, miR-125b might be a more specific predictive marker and a safe therapeutic target for treating patients with PE.
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spelling pubmed-72209442020-05-20 Elevated microRNA-125b inhibits cytotrophoblast invasion and impairs endothelial cell function in preeclampsia Li, Qinghua Han, Yangyang Xu, Peng Yin, Lingxuan Si, Yanru Zhang, Cuijuan Meng, Yuhan Feng, Weiguo Pan, Zhifang Gao, Zhiqin Li, Jie Yang, Weiwei Cell Death Discov Article Preeclampsia (PE) is a life-threatening disorder of human pregnancy affecting 5–8% of all pregnancies. Currently, PE remains an elusive complicated and heterogenous medical condition with no early marker or symptoms is recognized for this serious pregnancy complications. Here, we profiled the plasma miRNA expression patterns associated with preeclampsia and found 16 miRNAs were deregulated (p < 0.01) in patients who later developed PE. Circulating hsa-miR-125b was aberrantly upregulated in early pregnancy and significantly reduced after delivery in preeclampsia. We then investigated the underlying molecular mechanisms between miR-125b and PE in vitro. We found that upregulated miR-125b can target KCNA1 to inhibit trophoblast invasion in human trophoblast cells. Moreover, overexpression of miR-125b in HUVECs impaired endothelial cell function through GPC1. The findings indicated that upregulated miR-125b leads to impaired placentation, and an increased risk of preeclampsia, Our studies provide novel insights into the underlying mechanisms on the association of miR-125b in early pregnancy and risk of PE, miR-125b might be a more specific predictive marker and a safe therapeutic target for treating patients with PE. Nature Publishing Group UK 2020-05-13 /pmc/articles/PMC7220944/ /pubmed/32435510 http://dx.doi.org/10.1038/s41420-020-0269-0 Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Li, Qinghua
Han, Yangyang
Xu, Peng
Yin, Lingxuan
Si, Yanru
Zhang, Cuijuan
Meng, Yuhan
Feng, Weiguo
Pan, Zhifang
Gao, Zhiqin
Li, Jie
Yang, Weiwei
Elevated microRNA-125b inhibits cytotrophoblast invasion and impairs endothelial cell function in preeclampsia
title Elevated microRNA-125b inhibits cytotrophoblast invasion and impairs endothelial cell function in preeclampsia
title_full Elevated microRNA-125b inhibits cytotrophoblast invasion and impairs endothelial cell function in preeclampsia
title_fullStr Elevated microRNA-125b inhibits cytotrophoblast invasion and impairs endothelial cell function in preeclampsia
title_full_unstemmed Elevated microRNA-125b inhibits cytotrophoblast invasion and impairs endothelial cell function in preeclampsia
title_short Elevated microRNA-125b inhibits cytotrophoblast invasion and impairs endothelial cell function in preeclampsia
title_sort elevated microrna-125b inhibits cytotrophoblast invasion and impairs endothelial cell function in preeclampsia
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7220944/
https://www.ncbi.nlm.nih.gov/pubmed/32435510
http://dx.doi.org/10.1038/s41420-020-0269-0
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