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On-line Access: 2021-02-07

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 ORCID:

Jihua JIN

https://orcid.org/0000-0002-3450-1298

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Journal of Zhejiang University SCIENCE B 2021 Vol.22 No.2 P.165-170

http://doi.org/10.1631/jzus.B2000557


Mitochondrial fusion protein 2 regulates endoplasmic reticulum stress in preeclampsia


Author(s):  Dandan SUN, Hui ZHU, Ling AI, Hanbing WU, Yanting WU, Jihua JIN

Affiliation(s):  Department of Obstetrics, Jiaxing Municipal Maternal and Child Health Care Hospital, Jiaxing 314051, China; more

Corresponding email(s):   s18715296792@163.com

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Dandan SUN, Hui ZHU, Ling AI, Hanbing WU, Yanting WU, Jihua JIN. Mitochondrial fusion protein 2 regulates endoplasmic reticulum stress in preeclampsia[J]. Journal of Zhejiang University Science B, 2021, 22(2): 165-170.

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publisher="Zhejiang University Press & Springer",
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Abstract: 
Preeclampsia (PE) refers to a group of dysfunction syndromes associated with elevated blood pressure and proteinuria in women with previously normal blood pressure after 20 weeks of pregnancy, and it may be accompanied by symptoms including headache, vertigo, nausea and vomiting, and epigastric discomfort (Steegers et al., 2010). It is affected by a variety of risk factors and follows a distinctive disease progression, although its pathogenesis is still unknown. Upon termination of a PE pregnancy, the clinical symptoms of PE improve rapidly, suggesting that PE is a disease originating in the placenta. Recent studies have shown that excessive apoptosis of trophoblast cells and reduced trophoblast infiltration capacity can lead to superficial implantation of the placenta, a lack of spiral arteriole remodeling, and insufficient placental perfusion leading to placental ischemia and hypoxia, all of which are important factors that cause the onset of PE (Eddy et al., 2019). Therefore, there appears to be a close relationship between excessive trophoblast cell apoptosis and development of PE. Recently, increasing evidence has shown that in patients with PE, endoplasmic reticulum (ER) stress can cause trophoblast cell apoptosis, and this finding has become an important feature of the placental pathology of PE (Lorenzon-Ojea et al., 2020).

线粒体融合蛋白2(Mfn2)调节内质网应激在子痫前期的作用及其机制研究

目的:探究线粒体融合蛋白2(Mfn2)调控的内质网应激在子痫前期发生中的作用机制,为临床子痫前期的诊断和治疗提供参考。
创新点:本论文着眼于滋养层细胞的内质网应激在子痫前期中具有重要作用这一研究热点,通过对临床样本的检测和细胞水平的研究,阐明了Mfn2调控的内质网应激在子痫前期发生中的重要作用,初步确定该基因可能作为子痫前期的诊断和治疗靶点。该研究具有针对性强、创新高以及满足现实发展需求的意义。
方法:采用蛋白质免疫印迹法检测子痫前期和正常胎盘组织中Mfn2的表达差异;活细胞计数(CCK8)法、细胞划痕、Transwell、流式细胞术等实验方法分别用于检测Mfn2敲低对滋养层细胞JEG-3增殖、迁移、侵袭和凋亡的影响。蛋白质免疫印迹法检测内质网应激条件下滋养层细胞中Mfn2的表达,并通过CCK8、流式细胞术和超氧化物歧化酶(SOD)的测定检测Mfn2过表达后对内质网应激条件下滋养层细胞的细胞活力和氧化应激的改善情况。
结论:Mfn2在子痫前期胎盘组织中低表达,下调Mfn2可显著抑制滋养层细胞的增殖、迁移和侵袭。子痫前期下内质网应激将抑制Mfn2的表达,Mfn2的稳定表达可以通过调节内质网应激抑制子痫前期发生和发展。

关键词:线粒体融合蛋白2(Mfn2);内质网应激;子痫前期

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Reference

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