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2
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MicroRNA-30a-3p is overexpressed in the placentas of patients with preeclampsia and affects trophoblast invasion and apoptosis by its effects on IGF-1.微小 RNA-30a-3p 在子痫前期患者的胎盘中过度表达,并通过对 IGF-1 的影响影响滋养细胞的侵袭和凋亡。
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Aberrant TGFβ Signaling Contributes to Altered Trophoblast Differentiation in Preeclampsia.异常的转化生长因子β信号传导导致子痫前期中滋养层细胞分化改变。
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Variations of microRNAs in human placentas and plasma from preeclamptic pregnancy.子痫前期患者胎盘和血浆中微小 RNA 的变化。
Hypertension. 2014 Jun;63(6):1276-84. doi: 10.1161/HYPERTENSIONAHA.113.02647. Epub 2014 Mar 24.
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本文引用的文献

1
Cadmium and Reproductive Health in Women: A Systematic Review of the Epidemiologic Evidence.镉与女性生殖健康:流行病学证据的系统评价
Curr Environ Health Rep. 2014 Jun;1(2):172-184. doi: 10.1007/s40572-014-0013-0. Epub 2014 Mar 21.
2
Epigenetics and Preeclampsia: Defining Functional Epimutations in the Preeclamptic Placenta Related to the TGF-β Pathway.表观遗传学与子痫前期:定义子痫前期胎盘与转化生长因子-β信号通路相关的功能性表观突变
PLoS One. 2015 Oct 28;10(10):e0141294. doi: 10.1371/journal.pone.0141294. eCollection 2015.
3
Toxicological responses of environmental mixtures: Environmental metal mixtures display synergistic induction of metal-responsive and oxidative stress genes in placental cells.环境混合物的毒理学反应:环境金属混合物在胎盘细胞中对金属反应性和氧化应激基因表现出协同诱导作用。
Toxicol Appl Pharmacol. 2015 Dec 15;289(3):534-41. doi: 10.1016/j.taap.2015.10.005. Epub 2015 Oct 17.
4
Placental Cadmium Levels Are Associated with Increased Preeclampsia Risk.胎盘镉水平与子痫前期风险增加有关。
PLoS One. 2015 Sep 30;10(9):e0139341. doi: 10.1371/journal.pone.0139341. eCollection 2015.
5
The imbalance in expression of angiogenic and anti-angiogenic factors as candidate predictive biomarker in preeclampsia.血管生成因子与抗血管生成因子表达失衡作为子痫前期候选预测生物标志物的研究
Iran J Reprod Med. 2015 May;13(5):251-62.
6
Prenatal exposure to arsenic and cadmium impacts infectious disease-related genes within the glucocorticoid receptor signal transduction pathway.孕期暴露于砷和镉会影响糖皮质激素受体信号转导途径内与传染病相关的基因。
Int J Mol Sci. 2014 Dec 3;15(12):22374-91. doi: 10.3390/ijms151222374.
7
Pre-eclampsia part 1: current understanding of its pathophysiology.子痫前期 1 部分:对其病理生理学的现有理解。
Nat Rev Nephrol. 2014 Aug;10(8):466-80. doi: 10.1038/nrneph.2014.102. Epub 2014 Jul 8.
8
A review of the mechanism for poor placentation in early-onset preeclampsia: the role of autophagy in trophoblast invasion and vascular remodeling.早发型子痫前期胎盘形成不良机制的综述:自噬在滋养细胞侵袭和血管重塑中的作用
J Reprod Immunol. 2014 Mar;101-102:80-88. doi: 10.1016/j.jri.2013.06.002. Epub 2013 Aug 2.
9
The ERK1/2 signaling pathway regulates 11beta-hydroxysteroid dehydrogenase type 2 expression in human trophoblast cells through a transcriptional mechanism.ERK1/2 信号通路通过转录机制调节人滋养层细胞 11β-羟类固醇脱氢酶 2 的表达。
Biol Reprod. 2013 Oct 17;89(4):92. doi: 10.1095/biolreprod.113.110924. Print 2013 Oct.
10
Growth factors in preeclampsia: a vascular disease model. A failed vasodilation and angiogenic challenge from pregnancy onwards?先兆子痫中的生长因子:一种血管疾病模型。从怀孕开始,血管舒张和血管生成的挑战失败了吗?
Cytokine Growth Factor Rev. 2013 Oct;24(5):411-25. doi: 10.1016/j.cytogfr.2013.05.008. Epub 2013 Jun 22.

微小RNA作为子痫前期胎盘和镉处理的滋养层细胞中转化生长因子(TGF)-β信号通路的常见调节因子:环境、表观基因组与子痫前期之间的联系

miRNAs as common regulators of the transforming growth factor (TGF)-β pathway in the preeclamptic placenta and cadmium-treated trophoblasts: Links between the environment, the epigenome and preeclampsia.

作者信息

Brooks Samira A, Martin Elizabeth, Smeester Lisa, Grace Matthew R, Boggess Kim, Fry Rebecca C

机构信息

Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, 135 Dauer Drive, CB 7431, University of North Carolina, Chapel Hill, NC, USA.

Department of Obstetrics & Gynecology, University of North Carolina School of Medicine, University of North Carolina, Chapel Hill, NC, USA.

出版信息

Food Chem Toxicol. 2016 Dec;98(Pt A):50-57. doi: 10.1016/j.fct.2016.06.023. Epub 2016 Jun 29.

DOI:10.1016/j.fct.2016.06.023
PMID:27375191
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5156314/
Abstract

Preeclampsia (PE) is a pregnancy disorder characterized by high blood pressure and proteinuria that can cause adverse health effects in both mother and fetus. There is no current cure for PE other than delivery of the fetus/placenta. While the etiology is unknown, poor placentation due to aberrant signaling of growth and angiogenic factors has been postulated as a causal factor of PE. In addition, environmental contaminants, such as the metal cadmium (Cd), have been linked to placental toxicity and increased risk of developing PE. Here, we use a translational study design to investigate genomic and epigenomic alterations in both placentas and placental trophoblasts, focused on the angiogenesis-associated transforming growth factor-beta (TGF-β) pathway. Genes within the TGF-β pathway displayed increased expression in both the preeclamptic placenta and Cd-treated trophoblasts. In addition, miRNAs that target the TGF-β pathway were also significantly altered within the preeclamptic placenta and Cd-treated trophoblasts. Integrative analysis resulted in the identification of a subset of Cd-responsive miRNAs, including miR-26a and miR-155, common to preeclamptic placentas and Cd-treated trophoblasts. These miRNAs have previously been linked to PE and are predicted to regulate members of the TGF-β pathway. Results from this study provide future targets for PE treatment.

摘要

子痫前期(PE)是一种妊娠疾病,其特征为高血压和蛋白尿,可对母亲和胎儿的健康造成不良影响。除了娩出胎儿/胎盘外,目前尚无治疗PE的方法。虽然其病因尚不清楚,但生长和血管生成因子的异常信号传导导致的胎盘形成不良被认为是PE的一个致病因素。此外,环境污染物,如金属镉(Cd),与胎盘毒性和发生PE的风险增加有关。在此,我们采用转化研究设计,研究胎盘和胎盘滋养层细胞中的基因组和表观基因组改变,重点关注与血管生成相关的转化生长因子-β(TGF-β)途径。TGF-β途径中的基因在子痫前期胎盘和镉处理的滋养层细胞中均表现出表达增加。此外,靶向TGF-β途径的微小RNA(miRNA)在子痫前期胎盘和镉处理的滋养层细胞中也有显著改变。综合分析鉴定出了一组镉反应性miRNA,包括子痫前期胎盘和镉处理的滋养层细胞共有的miR-26a和miR-155。这些miRNA此前已与PE相关联,并预计可调节TGF-β途径的成员。本研究结果为PE治疗提供了未来的靶点。