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Alteration in methylation level at 11β-hydroxysteroid dehydrogenase type 2 gene promoter in infants born to preeclamptic women
BACKGROUND: Preeclampsia reduces placental expression and activity of 11β-hydroxysteroid dehydrogenase type 2 (HSD11B2), leading to an increase in fetal glucocordicoids. The latter has been proposed to be associated with low birth weight and high risk of metabolic diseases in later life of the offsp...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4363912/ https://www.ncbi.nlm.nih.gov/pubmed/25200528 http://dx.doi.org/10.1186/s12863-014-0096-5 |
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author | Hu, Wensheng Weng, Xiaoling Dong, Minyue Liu, Yun Li, Wenjuan Huang, Hefeng |
author_facet | Hu, Wensheng Weng, Xiaoling Dong, Minyue Liu, Yun Li, Wenjuan Huang, Hefeng |
author_sort | Hu, Wensheng |
collection | PubMed |
description | BACKGROUND: Preeclampsia reduces placental expression and activity of 11β-hydroxysteroid dehydrogenase type 2 (HSD11B2), leading to an increase in fetal glucocordicoids. The latter has been proposed to be associated with low birth weight and high risk of metabolic diseases in later life of the offspring. This investigation aims to delineate the alteration in methylation levels at CpG sites of HSD11B2 promoter. RESULTS: Methylation levels of HSD9-2, HSD9-3, HSD23-2 and HSD23-3 and the mean methylation level were significantly lower in preeclampsia than in normal pregnancy (P = 0.002, 0.031, 0.047 and 0.001, respectively and P < 0.001 in mean). The mean methylation level was significantly correlated with preeclampsia after the adjustment of birth weight, maternal age, gestational age at delivery and fetal gender (r = 0.325, P < 0.001). CONCLUSIONS: Preeclampsia reduced methylation level at fetal HSD11B2 promoter. A positive correlation existed between HSD11B2 promoter methylation and preeclampsia. Our findings suggest that the methyaltion status of HSD11B2 promoter is a potentially accessible biomarker for preeclampsia. However, further studies are required to address the mechanisms of thehypomethylation at HSD11B2 promoter and the significance of the hypomethylation in the development of metabolic diseases of the fetals born to preeclamptic women. |
format | Online Article Text |
id | pubmed-4363912 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-43639122015-03-19 Alteration in methylation level at 11β-hydroxysteroid dehydrogenase type 2 gene promoter in infants born to preeclamptic women Hu, Wensheng Weng, Xiaoling Dong, Minyue Liu, Yun Li, Wenjuan Huang, Hefeng BMC Genet Research Article BACKGROUND: Preeclampsia reduces placental expression and activity of 11β-hydroxysteroid dehydrogenase type 2 (HSD11B2), leading to an increase in fetal glucocordicoids. The latter has been proposed to be associated with low birth weight and high risk of metabolic diseases in later life of the offspring. This investigation aims to delineate the alteration in methylation levels at CpG sites of HSD11B2 promoter. RESULTS: Methylation levels of HSD9-2, HSD9-3, HSD23-2 and HSD23-3 and the mean methylation level were significantly lower in preeclampsia than in normal pregnancy (P = 0.002, 0.031, 0.047 and 0.001, respectively and P < 0.001 in mean). The mean methylation level was significantly correlated with preeclampsia after the adjustment of birth weight, maternal age, gestational age at delivery and fetal gender (r = 0.325, P < 0.001). CONCLUSIONS: Preeclampsia reduced methylation level at fetal HSD11B2 promoter. A positive correlation existed between HSD11B2 promoter methylation and preeclampsia. Our findings suggest that the methyaltion status of HSD11B2 promoter is a potentially accessible biomarker for preeclampsia. However, further studies are required to address the mechanisms of thehypomethylation at HSD11B2 promoter and the significance of the hypomethylation in the development of metabolic diseases of the fetals born to preeclamptic women. BioMed Central 2014-09-09 /pmc/articles/PMC4363912/ /pubmed/25200528 http://dx.doi.org/10.1186/s12863-014-0096-5 Text en Copyright © 2014 Hu et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. 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 Hu, Wensheng Weng, Xiaoling Dong, Minyue Liu, Yun Li, Wenjuan Huang, Hefeng Alteration in methylation level at 11β-hydroxysteroid dehydrogenase type 2 gene promoter in infants born to preeclamptic women |
title | Alteration in methylation level at 11β-hydroxysteroid dehydrogenase type 2 gene promoter in infants born to preeclamptic women |
title_full | Alteration in methylation level at 11β-hydroxysteroid dehydrogenase type 2 gene promoter in infants born to preeclamptic women |
title_fullStr | Alteration in methylation level at 11β-hydroxysteroid dehydrogenase type 2 gene promoter in infants born to preeclamptic women |
title_full_unstemmed | Alteration in methylation level at 11β-hydroxysteroid dehydrogenase type 2 gene promoter in infants born to preeclamptic women |
title_short | Alteration in methylation level at 11β-hydroxysteroid dehydrogenase type 2 gene promoter in infants born to preeclamptic women |
title_sort | alteration in methylation level at 11β-hydroxysteroid dehydrogenase type 2 gene promoter in infants born to preeclamptic women |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4363912/ https://www.ncbi.nlm.nih.gov/pubmed/25200528 http://dx.doi.org/10.1186/s12863-014-0096-5 |
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