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Long Non-Coding RNA Nuclear-Enriched Abundant Transcript 1 (NEAT1) Represses Proliferation of Trophoblast Cells in Rats with Preeclampsia via the MicroRNA-373/FLT1 Axis

BACKGROUND: Preeclampsia (PE) remains one of the primary causes of maternal morbidity and mortality worldwide. This study was designed to investigate the relevance of long non-coding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) and downstream molecules in trophoblast cell proliferatio...

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Autores principales: Teng, Lingling, Liu, Pingping, Song, Xiao, Wang, Hui, Sun, Jing, Yin, Zhongxia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7590520/
https://www.ncbi.nlm.nih.gov/pubmed/33093438
http://dx.doi.org/10.12659/MSM.927305
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author Teng, Lingling
Liu, Pingping
Song, Xiao
Wang, Hui
Sun, Jing
Yin, Zhongxia
author_facet Teng, Lingling
Liu, Pingping
Song, Xiao
Wang, Hui
Sun, Jing
Yin, Zhongxia
author_sort Teng, Lingling
collection PubMed
description BACKGROUND: Preeclampsia (PE) remains one of the primary causes of maternal morbidity and mortality worldwide. This study was designed to investigate the relevance of long non-coding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) and downstream molecules in trophoblast cell proliferation and apoptosis. MATERIAL/METHODS: NEAT1 expression in the placental tissues of rats with PE was analyzed by reverse transcriptionquantitative polymerase chain reaction. The role of NEAT in trophoblast cell proliferation, migration, invasion, and apoptosis was assessed by transfecting pcDNA-NEAT1 and siRNA-NEAT1 into trophoblast cells. The microRNA (miRNA) binding to NEAT1 and the genes targeted by the screened miRNAs were predicted by Starbase, and the mechanism of action of NEAT1 in PE was further investigated. RESULTS: The expression of NEAT1 lncRNA was markedly higher in placental samples of PE than control rats. Ectopic expression of NEAT1 repressed trophoblast cell proliferation, migration, invasion, and colony formation, but facilitated cell apoptosis, whereas NEAT1 downregulation resulted in the opposite effects. NEAT1 was found to act as a molecular sponge for miR-373, regulating Fms-like tyrosine kinase-1 (FLT-1) to modulate PE development. CONCLUSIONS: NEAT1 may contribute to PE development by regulating trophoblast cell proliferation and apoptosis. These findings may provide a new perspective for understanding the etiology and pathogenesis of PE.
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spelling pubmed-75905202020-10-28 Long Non-Coding RNA Nuclear-Enriched Abundant Transcript 1 (NEAT1) Represses Proliferation of Trophoblast Cells in Rats with Preeclampsia via the MicroRNA-373/FLT1 Axis Teng, Lingling Liu, Pingping Song, Xiao Wang, Hui Sun, Jing Yin, Zhongxia Med Sci Monit Animal Study BACKGROUND: Preeclampsia (PE) remains one of the primary causes of maternal morbidity and mortality worldwide. This study was designed to investigate the relevance of long non-coding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) and downstream molecules in trophoblast cell proliferation and apoptosis. MATERIAL/METHODS: NEAT1 expression in the placental tissues of rats with PE was analyzed by reverse transcriptionquantitative polymerase chain reaction. The role of NEAT in trophoblast cell proliferation, migration, invasion, and apoptosis was assessed by transfecting pcDNA-NEAT1 and siRNA-NEAT1 into trophoblast cells. The microRNA (miRNA) binding to NEAT1 and the genes targeted by the screened miRNAs were predicted by Starbase, and the mechanism of action of NEAT1 in PE was further investigated. RESULTS: The expression of NEAT1 lncRNA was markedly higher in placental samples of PE than control rats. Ectopic expression of NEAT1 repressed trophoblast cell proliferation, migration, invasion, and colony formation, but facilitated cell apoptosis, whereas NEAT1 downregulation resulted in the opposite effects. NEAT1 was found to act as a molecular sponge for miR-373, regulating Fms-like tyrosine kinase-1 (FLT-1) to modulate PE development. CONCLUSIONS: NEAT1 may contribute to PE development by regulating trophoblast cell proliferation and apoptosis. These findings may provide a new perspective for understanding the etiology and pathogenesis of PE. International Scientific Literature, Inc. 2020-10-23 /pmc/articles/PMC7590520/ /pubmed/33093438 http://dx.doi.org/10.12659/MSM.927305 Text en © Med Sci Monit, 2020 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) )
spellingShingle Animal Study
Teng, Lingling
Liu, Pingping
Song, Xiao
Wang, Hui
Sun, Jing
Yin, Zhongxia
Long Non-Coding RNA Nuclear-Enriched Abundant Transcript 1 (NEAT1) Represses Proliferation of Trophoblast Cells in Rats with Preeclampsia via the MicroRNA-373/FLT1 Axis
title Long Non-Coding RNA Nuclear-Enriched Abundant Transcript 1 (NEAT1) Represses Proliferation of Trophoblast Cells in Rats with Preeclampsia via the MicroRNA-373/FLT1 Axis
title_full Long Non-Coding RNA Nuclear-Enriched Abundant Transcript 1 (NEAT1) Represses Proliferation of Trophoblast Cells in Rats with Preeclampsia via the MicroRNA-373/FLT1 Axis
title_fullStr Long Non-Coding RNA Nuclear-Enriched Abundant Transcript 1 (NEAT1) Represses Proliferation of Trophoblast Cells in Rats with Preeclampsia via the MicroRNA-373/FLT1 Axis
title_full_unstemmed Long Non-Coding RNA Nuclear-Enriched Abundant Transcript 1 (NEAT1) Represses Proliferation of Trophoblast Cells in Rats with Preeclampsia via the MicroRNA-373/FLT1 Axis
title_short Long Non-Coding RNA Nuclear-Enriched Abundant Transcript 1 (NEAT1) Represses Proliferation of Trophoblast Cells in Rats with Preeclampsia via the MicroRNA-373/FLT1 Axis
title_sort long non-coding rna nuclear-enriched abundant transcript 1 (neat1) represses proliferation of trophoblast cells in rats with preeclampsia via the microrna-373/flt1 axis
topic Animal Study
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7590520/
https://www.ncbi.nlm.nih.gov/pubmed/33093438
http://dx.doi.org/10.12659/MSM.927305
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