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Expressions of VEGF-A and VEGFR-2 in placentae from GDM pregnancies

BACKGROUND: Gestational diabetes mellitus (GDM) is one of the most common medical complications of pregnancy, and has important health implications for mother and child. Changes in the fetoplacental vessels may predict those in the vasculature of the developing fetus, as these have been implicated i...

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Autores principales: Meng, Qian, Shao, Li, Luo, Xiucui, Mu, Yingping, Xu, Wen, Gao, Li, Xu, Haoqin, Cui, Yugui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5029036/
https://www.ncbi.nlm.nih.gov/pubmed/27645229
http://dx.doi.org/10.1186/s12958-016-0191-8
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author Meng, Qian
Shao, Li
Luo, Xiucui
Mu, Yingping
Xu, Wen
Gao, Li
Xu, Haoqin
Cui, Yugui
author_facet Meng, Qian
Shao, Li
Luo, Xiucui
Mu, Yingping
Xu, Wen
Gao, Li
Xu, Haoqin
Cui, Yugui
author_sort Meng, Qian
collection PubMed
description BACKGROUND: Gestational diabetes mellitus (GDM) is one of the most common medical complications of pregnancy, and has important health implications for mother and child. Changes in the fetoplacental vessels may predict those in the vasculature of the developing fetus, as these have been implicated in the pathogenesis of human GDM. This study aimed to determine the differences in the localization and expression level of VEGFA and VEGFR2 between placentas of women with GDM and placentas of normal pregnancies, which is the first step in elucidating the possible roles of VEGFA and VEGFR2 in the altered uteroplacental function resulting from maternal hyperglycaemia and ultimately in the manifestation of GDM. METHODS: The expressions of VEGFA and VEGFR2 mRNA and protein in 20 samples from each group were analyzed by real-time PCR, immunohistochemistry and Western blot. The placental blood barrier and angiogenesis were observed by the transmission electron microscopy (TEM) in10 GDM samples and ten controls. RESULTS: The expression levels of VEGFA and VEGFR2 mRNA and protein were significantly decreased in the GDM group (P < 0.05 or 0.01). Immunohistochemical analysis showed the reduced expression of VEGFA and VEGFR2 protein in GDM-affected placental tissues, and the degenerative alterations of the terminal villi vascular. CONCLUSION: The expressions of VEGFA and VEGFR-2 mRNAs and protein were reduced in GDM-affected placental tissues, suggesting that maternal GDM affects the pathophysiological function of placentas. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12958-016-0191-8) contains supplementary material, which is available to authorized users.
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spelling pubmed-50290362016-09-22 Expressions of VEGF-A and VEGFR-2 in placentae from GDM pregnancies Meng, Qian Shao, Li Luo, Xiucui Mu, Yingping Xu, Wen Gao, Li Xu, Haoqin Cui, Yugui Reprod Biol Endocrinol Research BACKGROUND: Gestational diabetes mellitus (GDM) is one of the most common medical complications of pregnancy, and has important health implications for mother and child. Changes in the fetoplacental vessels may predict those in the vasculature of the developing fetus, as these have been implicated in the pathogenesis of human GDM. This study aimed to determine the differences in the localization and expression level of VEGFA and VEGFR2 between placentas of women with GDM and placentas of normal pregnancies, which is the first step in elucidating the possible roles of VEGFA and VEGFR2 in the altered uteroplacental function resulting from maternal hyperglycaemia and ultimately in the manifestation of GDM. METHODS: The expressions of VEGFA and VEGFR2 mRNA and protein in 20 samples from each group were analyzed by real-time PCR, immunohistochemistry and Western blot. The placental blood barrier and angiogenesis were observed by the transmission electron microscopy (TEM) in10 GDM samples and ten controls. RESULTS: The expression levels of VEGFA and VEGFR2 mRNA and protein were significantly decreased in the GDM group (P < 0.05 or 0.01). Immunohistochemical analysis showed the reduced expression of VEGFA and VEGFR2 protein in GDM-affected placental tissues, and the degenerative alterations of the terminal villi vascular. CONCLUSION: The expressions of VEGFA and VEGFR-2 mRNAs and protein were reduced in GDM-affected placental tissues, suggesting that maternal GDM affects the pathophysiological function of placentas. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12958-016-0191-8) contains supplementary material, which is available to authorized users. BioMed Central 2016-09-20 /pmc/articles/PMC5029036/ /pubmed/27645229 http://dx.doi.org/10.1186/s12958-016-0191-8 Text en © The Author(s). 2016 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
Meng, Qian
Shao, Li
Luo, Xiucui
Mu, Yingping
Xu, Wen
Gao, Li
Xu, Haoqin
Cui, Yugui
Expressions of VEGF-A and VEGFR-2 in placentae from GDM pregnancies
title Expressions of VEGF-A and VEGFR-2 in placentae from GDM pregnancies
title_full Expressions of VEGF-A and VEGFR-2 in placentae from GDM pregnancies
title_fullStr Expressions of VEGF-A and VEGFR-2 in placentae from GDM pregnancies
title_full_unstemmed Expressions of VEGF-A and VEGFR-2 in placentae from GDM pregnancies
title_short Expressions of VEGF-A and VEGFR-2 in placentae from GDM pregnancies
title_sort expressions of vegf-a and vegfr-2 in placentae from gdm pregnancies
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5029036/
https://www.ncbi.nlm.nih.gov/pubmed/27645229
http://dx.doi.org/10.1186/s12958-016-0191-8
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