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DNA 甲基化重编程的催产素受体是子痫前期胎盘血管对催产素不敏感的基础。

DNA methylation-reprogrammed oxytocin receptor underlies insensitivity to oxytocin in pre-eclamptic placental vasculature.

机构信息

Institute for Fetology and Department of Obstetrics and Gynecology, First Hospital of Soochow University, Suzhou, China.

Department of Obstetrics and Gynecology, Affiliated Suzhou Hospital of Nanjing University of Chinese Medicine, Suzhou, China.

出版信息

J Cell Mol Med. 2019 Jun;23(6):4118-4126. doi: 10.1111/jcmm.14299. Epub 2019 Apr 4.

DOI:10.1111/jcmm.14299
PMID:30950195
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6533468/
Abstract

Pre-eclampsia is associated with inadequate placental blood flow and placental ischaemia. Placental vascular tone is essential for maintaining adequate placental blood flow. Oxytocin is increased in placental system at late pregnancy and onset of labour, and presented strongly concentration-dependent contractions in placental vascular, suggesting that oxytocin could be involved in regulating placental vascular tone and circulation. However, information about the reactivity of oxytocin in pre-eclamptic placental vasculature is limited. This study used a large number of human placentas to reveal the pathophysiological changes and its underlying mechanisms of oxytocin-induced vasoconstrictions in placental vessels under pre-eclamptic condition. Present study found that oxytocin-induced contractions were significantly decreased in human pre-eclamptic placental vasculature, associated with a deactivated transcription of oxytocin receptor gene. The deactivated oxytocin receptor gene transcription was ascribed to a relatively higher DNA methylation status of CpG islands in oxytocin receptor gene promoter. This study was first to reveal that a hyper-methylation of CpG islands in oxytocin receptor gene promoter, leading to a relatively low pattern of oxytocin receptor expression, was responsible for the decreased sensitivity of oxytocin in pre-eclamptic placental vessels.

摘要

子痫前期与胎盘血流不足和胎盘缺血有关。胎盘血管张力对于维持适当的胎盘血流至关重要。在妊娠晚期和分娩开始时，催产素在胎盘系统中增加，并呈现出强烈的浓度依赖性收缩，表明催产素可能参与调节胎盘血管张力和循环。然而，关于催产素在子痫前期胎盘血管中的反应性的信息有限。本研究使用大量的人胎盘来揭示在子痫前期条件下，催产素诱导的血管收缩的病理生理变化及其潜在机制。本研究发现，催产素诱导的收缩在人子痫前期胎盘血管中显著减少，与催产素受体基因的转录失活有关。失活的催产素受体基因转录归因于催产素受体基因启动子中 CpG 岛的相对较高的 DNA 甲基化状态。本研究首次揭示，催产素受体基因启动子中 CpG 岛的高甲基化导致催产素受体表达模式相对较低，这是导致子痫前期胎盘血管中催产素敏感性降低的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eb4/6533468/e881dbfd8eb8/JCMM-23-4118-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eb4/6533468/73bc9fc2d56e/JCMM-23-4118-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eb4/6533468/8e35d4f174cf/JCMM-23-4118-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eb4/6533468/4c0935d6c820/JCMM-23-4118-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eb4/6533468/e881dbfd8eb8/JCMM-23-4118-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eb4/6533468/73bc9fc2d56e/JCMM-23-4118-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eb4/6533468/8e35d4f174cf/JCMM-23-4118-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eb4/6533468/4c0935d6c820/JCMM-23-4118-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eb4/6533468/e881dbfd8eb8/JCMM-23-4118-g004.jpg

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