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Aquaporin-8 overexpression is involved in vascular structure and function changes in placentas of gestational diabetes mellitus patients
To study the role and mechanism of aquaporin-8 (AQP8) in placental vascular development in gestational diabetes mellitus (GDM), hematoxylin–eosin staining and immunohistochemistry were utilized to analyze the histopathological changes in placentas in GDM patients. Transwell, CCK-8, and tube formatio...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
De Gruyter
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9664169/ https://www.ncbi.nlm.nih.gov/pubmed/36448064 http://dx.doi.org/10.1515/biol-2022-0522 |
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author | Shan, Yanxing Cui, Jiawen Kang, Xinyi Tang, Weichun Lu, Yiling Gao, Ying Chen, Liping |
author_facet | Shan, Yanxing Cui, Jiawen Kang, Xinyi Tang, Weichun Lu, Yiling Gao, Ying Chen, Liping |
author_sort | Shan, Yanxing |
collection | PubMed |
description | To study the role and mechanism of aquaporin-8 (AQP8) in placental vascular development in gestational diabetes mellitus (GDM), hematoxylin–eosin staining and immunohistochemistry were utilized to analyze the histopathological changes in placentas in GDM patients. Transwell, CCK-8, and tube formation assays were performed to examine cell migration, proliferation, and tube formation. AQP8, vascular cell adhesion molecule 1 (VCAM-1), tumor necrosis factor alpha (TNF)-α, and vascular endothelial growth factor (VEGF)-A expression levels were investigated. Relative to the control group, the placentas in the GDM group showed morphological changes, the number of microvessels in the placental villi arterioles was significantly higher, and the area of microvessels in the arterioles of placental villi was significantly lower. The expression levels of VCAM-1, TNF-α, VEGF-A, and AQP8 in the GDM placentas and human umbilical vein endothelial cells (HUVECs) stimulated by high glucose were significantly higher than those in the control group, and AQP8 was located in placental endothelial cells. Overexpression of glucose and AQP8 inhibited tube formation, migration, and proliferation in HUVECs. High glucose levels can induce dysfunction in vascular endothelial cells and lead to pathological changes in the placental vascular structure in GDM. AQP8 overexpression in placental GDM can inhibit endothelial cell behavior, cause endothelial cell dysfunction, and further participate in the occurrence and development of GDM placental vascular lesions. |
format | Online Article Text |
id | pubmed-9664169 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | De Gruyter |
record_format | MEDLINE/PubMed |
spelling | pubmed-96641692022-11-28 Aquaporin-8 overexpression is involved in vascular structure and function changes in placentas of gestational diabetes mellitus patients Shan, Yanxing Cui, Jiawen Kang, Xinyi Tang, Weichun Lu, Yiling Gao, Ying Chen, Liping Open Life Sci Research Article To study the role and mechanism of aquaporin-8 (AQP8) in placental vascular development in gestational diabetes mellitus (GDM), hematoxylin–eosin staining and immunohistochemistry were utilized to analyze the histopathological changes in placentas in GDM patients. Transwell, CCK-8, and tube formation assays were performed to examine cell migration, proliferation, and tube formation. AQP8, vascular cell adhesion molecule 1 (VCAM-1), tumor necrosis factor alpha (TNF)-α, and vascular endothelial growth factor (VEGF)-A expression levels were investigated. Relative to the control group, the placentas in the GDM group showed morphological changes, the number of microvessels in the placental villi arterioles was significantly higher, and the area of microvessels in the arterioles of placental villi was significantly lower. The expression levels of VCAM-1, TNF-α, VEGF-A, and AQP8 in the GDM placentas and human umbilical vein endothelial cells (HUVECs) stimulated by high glucose were significantly higher than those in the control group, and AQP8 was located in placental endothelial cells. Overexpression of glucose and AQP8 inhibited tube formation, migration, and proliferation in HUVECs. High glucose levels can induce dysfunction in vascular endothelial cells and lead to pathological changes in the placental vascular structure in GDM. AQP8 overexpression in placental GDM can inhibit endothelial cell behavior, cause endothelial cell dysfunction, and further participate in the occurrence and development of GDM placental vascular lesions. De Gruyter 2022-11-14 /pmc/articles/PMC9664169/ /pubmed/36448064 http://dx.doi.org/10.1515/biol-2022-0522 Text en © 2022 Yanxing Shan et al., published by De Gruyter https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 International License. |
spellingShingle | Research Article Shan, Yanxing Cui, Jiawen Kang, Xinyi Tang, Weichun Lu, Yiling Gao, Ying Chen, Liping Aquaporin-8 overexpression is involved in vascular structure and function changes in placentas of gestational diabetes mellitus patients |
title | Aquaporin-8 overexpression is involved in vascular structure and function changes in placentas of gestational diabetes mellitus patients |
title_full | Aquaporin-8 overexpression is involved in vascular structure and function changes in placentas of gestational diabetes mellitus patients |
title_fullStr | Aquaporin-8 overexpression is involved in vascular structure and function changes in placentas of gestational diabetes mellitus patients |
title_full_unstemmed | Aquaporin-8 overexpression is involved in vascular structure and function changes in placentas of gestational diabetes mellitus patients |
title_short | Aquaporin-8 overexpression is involved in vascular structure and function changes in placentas of gestational diabetes mellitus patients |
title_sort | aquaporin-8 overexpression is involved in vascular structure and function changes in placentas of gestational diabetes mellitus patients |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9664169/ https://www.ncbi.nlm.nih.gov/pubmed/36448064 http://dx.doi.org/10.1515/biol-2022-0522 |
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