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Effect of lncRNA‐ATB/miR‐651‐3p/Yin Yang 1 pathway on trophoblast‐endothelial cell interaction networks

Our previous studies have confirmed that lncRNA‐ATB may be involved in the pathogenesis of preeclampsia, however, it is uncertain whether lncRNA‐ATB influence the interaction between trophoblast and endothelial cells, which is crucial to the uterine spiral artery remodelling. Scratch wound healing a...

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Autores principales: Yin, Yangxue, Zhang, Jiashuo, Yu, Hongbiao, Liu, Min, Zheng, Xuelian, Zhou, Rong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8184718/
https://www.ncbi.nlm.nih.gov/pubmed/33942988
http://dx.doi.org/10.1111/jcmm.16550
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author Yin, Yangxue
Zhang, Jiashuo
Yu, Hongbiao
Liu, Min
Zheng, Xuelian
Zhou, Rong
author_facet Yin, Yangxue
Zhang, Jiashuo
Yu, Hongbiao
Liu, Min
Zheng, Xuelian
Zhou, Rong
author_sort Yin, Yangxue
collection PubMed
description Our previous studies have confirmed that lncRNA‐ATB may be involved in the pathogenesis of preeclampsia, however, it is uncertain whether lncRNA‐ATB influence the interaction between trophoblast and endothelial cells, which is crucial to the uterine spiral artery remodelling. Scratch wound healing and transwell invasion assay were conducted to test the migration and invasion of trophoblast cells. Co‐culture model was used to simulate the physiological environment in vivo. The expression levels of lncRNA‐ATB were analyzed in placenta tissues from healthy pregnant women and preeclampsia patients. Subsequently, the binding site of lncRNA‐ATB and miR‐651‐3p was verified using dual‐luciferase reporter assay, and the rescue experiment was used to study the effects of these two on the biological function. The direct effects of miR‐651‐3p and Yin Yang 1 (YY1) were verified using similar methods. LncRNA‐ATB was found to be down‐regulated in the placenta of preeclampsia patients. LncRNA‐ATB knockdown decreased trophoblast migration, invasion and colocalisation with human umbilical vein endothelial cells. MiR‐651‐3p was a direct target of lncRNA‐ATB and they had opposite effects. Moreover, the expression of lncRNA‐ATB and miR‐651‐3p in placental tissues was negatively correlated. MiR‐651‐3p has been confirmed to directly target the 3′ untranslated region of YY1. The inhibitory effects of YY1 low expression on biological function was rescued by miR‐651‐3p depletion. Western blot analysis showed that lncRNA‐ATB could regulate YY1 expression by sponging miR‐651‐3p. LncRNA‐ATB functioned as a competitive endogenous RNA of miR‐651‐3p to regulate YY1 on progress of spiral artery remodelling.
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spelling pubmed-81847182021-06-15 Effect of lncRNA‐ATB/miR‐651‐3p/Yin Yang 1 pathway on trophoblast‐endothelial cell interaction networks Yin, Yangxue Zhang, Jiashuo Yu, Hongbiao Liu, Min Zheng, Xuelian Zhou, Rong J Cell Mol Med Original Articles Our previous studies have confirmed that lncRNA‐ATB may be involved in the pathogenesis of preeclampsia, however, it is uncertain whether lncRNA‐ATB influence the interaction between trophoblast and endothelial cells, which is crucial to the uterine spiral artery remodelling. Scratch wound healing and transwell invasion assay were conducted to test the migration and invasion of trophoblast cells. Co‐culture model was used to simulate the physiological environment in vivo. The expression levels of lncRNA‐ATB were analyzed in placenta tissues from healthy pregnant women and preeclampsia patients. Subsequently, the binding site of lncRNA‐ATB and miR‐651‐3p was verified using dual‐luciferase reporter assay, and the rescue experiment was used to study the effects of these two on the biological function. The direct effects of miR‐651‐3p and Yin Yang 1 (YY1) were verified using similar methods. LncRNA‐ATB was found to be down‐regulated in the placenta of preeclampsia patients. LncRNA‐ATB knockdown decreased trophoblast migration, invasion and colocalisation with human umbilical vein endothelial cells. MiR‐651‐3p was a direct target of lncRNA‐ATB and they had opposite effects. Moreover, the expression of lncRNA‐ATB and miR‐651‐3p in placental tissues was negatively correlated. MiR‐651‐3p has been confirmed to directly target the 3′ untranslated region of YY1. The inhibitory effects of YY1 low expression on biological function was rescued by miR‐651‐3p depletion. Western blot analysis showed that lncRNA‐ATB could regulate YY1 expression by sponging miR‐651‐3p. LncRNA‐ATB functioned as a competitive endogenous RNA of miR‐651‐3p to regulate YY1 on progress of spiral artery remodelling. John Wiley and Sons Inc. 2021-05-04 2021-06 /pmc/articles/PMC8184718/ /pubmed/33942988 http://dx.doi.org/10.1111/jcmm.16550 Text en © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://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
Yin, Yangxue
Zhang, Jiashuo
Yu, Hongbiao
Liu, Min
Zheng, Xuelian
Zhou, Rong
Effect of lncRNA‐ATB/miR‐651‐3p/Yin Yang 1 pathway on trophoblast‐endothelial cell interaction networks
title Effect of lncRNA‐ATB/miR‐651‐3p/Yin Yang 1 pathway on trophoblast‐endothelial cell interaction networks
title_full Effect of lncRNA‐ATB/miR‐651‐3p/Yin Yang 1 pathway on trophoblast‐endothelial cell interaction networks
title_fullStr Effect of lncRNA‐ATB/miR‐651‐3p/Yin Yang 1 pathway on trophoblast‐endothelial cell interaction networks
title_full_unstemmed Effect of lncRNA‐ATB/miR‐651‐3p/Yin Yang 1 pathway on trophoblast‐endothelial cell interaction networks
title_short Effect of lncRNA‐ATB/miR‐651‐3p/Yin Yang 1 pathway on trophoblast‐endothelial cell interaction networks
title_sort effect of lncrna‐atb/mir‐651‐3p/yin yang 1 pathway on trophoblast‐endothelial cell interaction networks
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8184718/
https://www.ncbi.nlm.nih.gov/pubmed/33942988
http://dx.doi.org/10.1111/jcmm.16550
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