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Maspin impairs the function of endothelial cells: an implying pathway of preeclampsia
BACKGROUD: Widespread endothelial injury contributes to the occurrence of preeclampsia. Maspin, first identified as a tumor suppressor, plays a critical role in cell invasion and angiogenesis. Our previous studies found that the expression of maspin was increased in preeclampsic placenta. In this re...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5622509/ https://www.ncbi.nlm.nih.gov/pubmed/28962595 http://dx.doi.org/10.1186/s12884-017-1525-z |
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author | Zhang, Ying Liu, Hao Shi, Xinwei Qiao, Fuyuan Zeng, Wanjiang Feng, Ling Deng, Dongrui Liu, Haiyi Wu, Yuanyuan |
author_facet | Zhang, Ying Liu, Hao Shi, Xinwei Qiao, Fuyuan Zeng, Wanjiang Feng, Ling Deng, Dongrui Liu, Haiyi Wu, Yuanyuan |
author_sort | Zhang, Ying |
collection | PubMed |
description | BACKGROUD: Widespread endothelial injury contributes to the occurrence of preeclampsia. Maspin, first identified as a tumor suppressor, plays a critical role in cell invasion and angiogenesis. Our previous studies found that the expression of maspin was increased in preeclampsic placenta. In this research, we studied the function of human umbilical vein endothelial cells (HUVECs) to explore the role and possible mechanism of maspin gene in the pathogenesis of preeclampsia. METHODS: HUVECs were treated with different concentration of recombinant human maspin protein (r-maspin) during normoxia and hypoxia, we detected the proliferation, apoptosis, migration and tube formation of HUVECs. We also assessed nitride oxide (NO) synthesis and the expression of matrix metalloproteinase 2 (MMP2) to further explore the underlying molecular mechanism. RESULTS: There was only slight maspin expression at mRNA level in HUVECs. Treated HUVECs with r-maspin, the proliferation of HUVECs was significantly promoted both under normoxia and hypoxia. The tubes formed by HUVECs were significantly inhibited and NO synthesis was significantly reduced by r-maspin. Meantime, r-maspin also inhibited MMP2 expression and activity in HUVECs. However, there was no significant change in the migration and apoptosis of HUVECs. CONCLUSIONS: Maspin may be an important participant for mediating endothelial function and ultimately leads to the occurence of preeclamsia. |
format | Online Article Text |
id | pubmed-5622509 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-56225092017-10-11 Maspin impairs the function of endothelial cells: an implying pathway of preeclampsia Zhang, Ying Liu, Hao Shi, Xinwei Qiao, Fuyuan Zeng, Wanjiang Feng, Ling Deng, Dongrui Liu, Haiyi Wu, Yuanyuan BMC Pregnancy Childbirth Research Article BACKGROUD: Widespread endothelial injury contributes to the occurrence of preeclampsia. Maspin, first identified as a tumor suppressor, plays a critical role in cell invasion and angiogenesis. Our previous studies found that the expression of maspin was increased in preeclampsic placenta. In this research, we studied the function of human umbilical vein endothelial cells (HUVECs) to explore the role and possible mechanism of maspin gene in the pathogenesis of preeclampsia. METHODS: HUVECs were treated with different concentration of recombinant human maspin protein (r-maspin) during normoxia and hypoxia, we detected the proliferation, apoptosis, migration and tube formation of HUVECs. We also assessed nitride oxide (NO) synthesis and the expression of matrix metalloproteinase 2 (MMP2) to further explore the underlying molecular mechanism. RESULTS: There was only slight maspin expression at mRNA level in HUVECs. Treated HUVECs with r-maspin, the proliferation of HUVECs was significantly promoted both under normoxia and hypoxia. The tubes formed by HUVECs were significantly inhibited and NO synthesis was significantly reduced by r-maspin. Meantime, r-maspin also inhibited MMP2 expression and activity in HUVECs. However, there was no significant change in the migration and apoptosis of HUVECs. CONCLUSIONS: Maspin may be an important participant for mediating endothelial function and ultimately leads to the occurence of preeclamsia. BioMed Central 2017-09-29 /pmc/articles/PMC5622509/ /pubmed/28962595 http://dx.doi.org/10.1186/s12884-017-1525-z Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Zhang, Ying Liu, Hao Shi, Xinwei Qiao, Fuyuan Zeng, Wanjiang Feng, Ling Deng, Dongrui Liu, Haiyi Wu, Yuanyuan Maspin impairs the function of endothelial cells: an implying pathway of preeclampsia |
title | Maspin impairs the function of endothelial cells: an implying pathway of preeclampsia |
title_full | Maspin impairs the function of endothelial cells: an implying pathway of preeclampsia |
title_fullStr | Maspin impairs the function of endothelial cells: an implying pathway of preeclampsia |
title_full_unstemmed | Maspin impairs the function of endothelial cells: an implying pathway of preeclampsia |
title_short | Maspin impairs the function of endothelial cells: an implying pathway of preeclampsia |
title_sort | maspin impairs the function of endothelial cells: an implying pathway of preeclampsia |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5622509/ https://www.ncbi.nlm.nih.gov/pubmed/28962595 http://dx.doi.org/10.1186/s12884-017-1525-z |
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