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Reduced Expression of Enac in Placenta Tissues of Patients with Severe Preeclampsia Is Related to Compromised Trophoblastic Cell Migration and Invasion during Pregnancy

The purpose of the study is to investigate the expression of epithelial sodium channel (ENaC) in normal pregnancy and severe preeclampsia placenta and to explore the underlying mechanism of the relationship between the altered ENaC expression and onset of preeclampsia. Reverse transcription polymera...

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Detalles Bibliográficos
Autores principales: Wang, Shan, He, Guolin, Yang, Yue, Liu, Ying, Diao, Ruiying, Sheng, Kai, Liu, Xinghui, Xu, Wenming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3747050/
https://www.ncbi.nlm.nih.gov/pubmed/23977235
http://dx.doi.org/10.1371/journal.pone.0072153
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author Wang, Shan
He, Guolin
Yang, Yue
Liu, Ying
Diao, Ruiying
Sheng, Kai
Liu, Xinghui
Xu, Wenming
author_facet Wang, Shan
He, Guolin
Yang, Yue
Liu, Ying
Diao, Ruiying
Sheng, Kai
Liu, Xinghui
Xu, Wenming
author_sort Wang, Shan
collection PubMed
description The purpose of the study is to investigate the expression of epithelial sodium channel (ENaC) in normal pregnancy and severe preeclampsia placenta and to explore the underlying mechanism of the relationship between the altered ENaC expression and onset of preeclampsia. Reverse transcription polymerase chain reaction (RT-PCR) and Western blot were used to check epithelial sodium channel subunits expression in mRNA and protein level in first term and full term placental tissue. ENaCα specific RNAi were used to knockdown ENaC expression and cell invasion and migration assay were used to check whether reduced expression of ENaC can compromise trophoblast cell function. The result showed that ENaCα was highly expressed in first term placental trophoblast cells; while EnaCβ was highly expressed in full term placenta. Knockdown ENaCα expression by using small interfering RNA reduced the invasive and migration abilities of HTR-8/SVneo cell. Real time-PCR and Western blot analysis showed that the expression levels of ENaCβ were also significantly lower in severe preeclampsia compared with normal pregnancy. It is concluded that the ENaC played an important role in trophoblast cell invasion and migration. Reduced expression and activity of epithelial sodium channel in trophoblast cells may be involved in the pathogenesis of preeclampsia.
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spelling pubmed-37470502013-08-23 Reduced Expression of Enac in Placenta Tissues of Patients with Severe Preeclampsia Is Related to Compromised Trophoblastic Cell Migration and Invasion during Pregnancy Wang, Shan He, Guolin Yang, Yue Liu, Ying Diao, Ruiying Sheng, Kai Liu, Xinghui Xu, Wenming PLoS One Research Article The purpose of the study is to investigate the expression of epithelial sodium channel (ENaC) in normal pregnancy and severe preeclampsia placenta and to explore the underlying mechanism of the relationship between the altered ENaC expression and onset of preeclampsia. Reverse transcription polymerase chain reaction (RT-PCR) and Western blot were used to check epithelial sodium channel subunits expression in mRNA and protein level in first term and full term placental tissue. ENaCα specific RNAi were used to knockdown ENaC expression and cell invasion and migration assay were used to check whether reduced expression of ENaC can compromise trophoblast cell function. The result showed that ENaCα was highly expressed in first term placental trophoblast cells; while EnaCβ was highly expressed in full term placenta. Knockdown ENaCα expression by using small interfering RNA reduced the invasive and migration abilities of HTR-8/SVneo cell. Real time-PCR and Western blot analysis showed that the expression levels of ENaCβ were also significantly lower in severe preeclampsia compared with normal pregnancy. It is concluded that the ENaC played an important role in trophoblast cell invasion and migration. Reduced expression and activity of epithelial sodium channel in trophoblast cells may be involved in the pathogenesis of preeclampsia. Public Library of Science 2013-08-19 /pmc/articles/PMC3747050/ /pubmed/23977235 http://dx.doi.org/10.1371/journal.pone.0072153 Text en © 2013 Wang et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Wang, Shan
He, Guolin
Yang, Yue
Liu, Ying
Diao, Ruiying
Sheng, Kai
Liu, Xinghui
Xu, Wenming
Reduced Expression of Enac in Placenta Tissues of Patients with Severe Preeclampsia Is Related to Compromised Trophoblastic Cell Migration and Invasion during Pregnancy
title Reduced Expression of Enac in Placenta Tissues of Patients with Severe Preeclampsia Is Related to Compromised Trophoblastic Cell Migration and Invasion during Pregnancy
title_full Reduced Expression of Enac in Placenta Tissues of Patients with Severe Preeclampsia Is Related to Compromised Trophoblastic Cell Migration and Invasion during Pregnancy
title_fullStr Reduced Expression of Enac in Placenta Tissues of Patients with Severe Preeclampsia Is Related to Compromised Trophoblastic Cell Migration and Invasion during Pregnancy
title_full_unstemmed Reduced Expression of Enac in Placenta Tissues of Patients with Severe Preeclampsia Is Related to Compromised Trophoblastic Cell Migration and Invasion during Pregnancy
title_short Reduced Expression of Enac in Placenta Tissues of Patients with Severe Preeclampsia Is Related to Compromised Trophoblastic Cell Migration and Invasion during Pregnancy
title_sort reduced expression of enac in placenta tissues of patients with severe preeclampsia is related to compromised trophoblastic cell migration and invasion during pregnancy
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3747050/
https://www.ncbi.nlm.nih.gov/pubmed/23977235
http://dx.doi.org/10.1371/journal.pone.0072153
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