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High temperature requirement A1 in placental tissues and serum from pre-eclamptic pregnancies with or without fetal growth restriction
INTRODUCTION: Pre-eclampsia (PE) is the most serious syndrome of human pregnancy and it is potentially life-threatening for both mother and fetus. The aim of the study was to identify the role of high temperature requirement A1 (HtrA1) in pre-eclampsia. MATERIAL AND METHODS: One hundred consecutive...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Termedia Publishing House
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3776172/ https://www.ncbi.nlm.nih.gov/pubmed/24049530 http://dx.doi.org/10.5114/aoms.2013.34989 |
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author | Zong, Lu Wang, Lijuan Huang, Pu Shao, Wenyu Song, Yu Gou, Wenli |
author_facet | Zong, Lu Wang, Lijuan Huang, Pu Shao, Wenyu Song, Yu Gou, Wenli |
author_sort | Zong, Lu |
collection | PubMed |
description | INTRODUCTION: Pre-eclampsia (PE) is the most serious syndrome of human pregnancy and it is potentially life-threatening for both mother and fetus. The aim of the study was to identify the role of high temperature requirement A1 (HtrA1) in pre-eclampsia. MATERIAL AND METHODS: One hundred consecutive pregnancies complicated by PE and 100 normal controls were included in our study. The changes in serum HtrA1 and fetal growth restriction were recorded. The placentae after delivery was also obtained for laboratory analyses. RESULTS: High temperature requirement A1 expressed positively in all placenta tissues, but showed higher expression from control, PE with AGA (pre-eclamptic pregnancies with appropriate-for-gestational-age newborns) to PE with fetal growth restriction (FGR) groups. Early-onset PE happened more frequently while in PE with AGA, late-onset PE was more common. Additionally, we found that only during ∼28-32 gestational weeks, sera HtrA1 level of PE with AGA and PE with FGR was increased significantly compared with the control group (p < 0.05). In contrast, there was no significant difference between groups in other gestational ages in the third trimester (p > 0.05). CONCLUSIONS: HtrA1 could potentially affect trophoblast migration and invasion during placentation, resulting in the shallow invasion noted in pre-eclampsia. HtrA1 may play an important role in the etiology and severity of PE and FGR. But the actual mechanism still needs deep research. |
format | Online Article Text |
id | pubmed-3776172 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Termedia Publishing House |
record_format | MEDLINE/PubMed |
spelling | pubmed-37761722013-09-18 High temperature requirement A1 in placental tissues and serum from pre-eclamptic pregnancies with or without fetal growth restriction Zong, Lu Wang, Lijuan Huang, Pu Shao, Wenyu Song, Yu Gou, Wenli Arch Med Sci Clinical Research INTRODUCTION: Pre-eclampsia (PE) is the most serious syndrome of human pregnancy and it is potentially life-threatening for both mother and fetus. The aim of the study was to identify the role of high temperature requirement A1 (HtrA1) in pre-eclampsia. MATERIAL AND METHODS: One hundred consecutive pregnancies complicated by PE and 100 normal controls were included in our study. The changes in serum HtrA1 and fetal growth restriction were recorded. The placentae after delivery was also obtained for laboratory analyses. RESULTS: High temperature requirement A1 expressed positively in all placenta tissues, but showed higher expression from control, PE with AGA (pre-eclamptic pregnancies with appropriate-for-gestational-age newborns) to PE with fetal growth restriction (FGR) groups. Early-onset PE happened more frequently while in PE with AGA, late-onset PE was more common. Additionally, we found that only during ∼28-32 gestational weeks, sera HtrA1 level of PE with AGA and PE with FGR was increased significantly compared with the control group (p < 0.05). In contrast, there was no significant difference between groups in other gestational ages in the third trimester (p > 0.05). CONCLUSIONS: HtrA1 could potentially affect trophoblast migration and invasion during placentation, resulting in the shallow invasion noted in pre-eclampsia. HtrA1 may play an important role in the etiology and severity of PE and FGR. But the actual mechanism still needs deep research. Termedia Publishing House 2013-04-30 2013-08-30 /pmc/articles/PMC3776172/ /pubmed/24049530 http://dx.doi.org/10.5114/aoms.2013.34989 Text en Copyright © 2013 Termedia & Banach http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Clinical Research Zong, Lu Wang, Lijuan Huang, Pu Shao, Wenyu Song, Yu Gou, Wenli High temperature requirement A1 in placental tissues and serum from pre-eclamptic pregnancies with or without fetal growth restriction |
title | High temperature requirement A1 in placental tissues and serum from pre-eclamptic pregnancies with or without fetal growth restriction |
title_full | High temperature requirement A1 in placental tissues and serum from pre-eclamptic pregnancies with or without fetal growth restriction |
title_fullStr | High temperature requirement A1 in placental tissues and serum from pre-eclamptic pregnancies with or without fetal growth restriction |
title_full_unstemmed | High temperature requirement A1 in placental tissues and serum from pre-eclamptic pregnancies with or without fetal growth restriction |
title_short | High temperature requirement A1 in placental tissues and serum from pre-eclamptic pregnancies with or without fetal growth restriction |
title_sort | high temperature requirement a1 in placental tissues and serum from pre-eclamptic pregnancies with or without fetal growth restriction |
topic | Clinical Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3776172/ https://www.ncbi.nlm.nih.gov/pubmed/24049530 http://dx.doi.org/10.5114/aoms.2013.34989 |
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