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Pregnancy
Published in T. Yee Khong, Annie N. Y. Cheung, Wenxin Zheng, Richard Wing-Cheuk Wong, Hao Chen, Diagnostic Endometrial Pathology, 2019
T. Yee Khong, Annie N. Y. Cheung, Wenxin Zheng
To emphasise the disordered migration of extravillous trophoblast in these pregnancy complications, endovascular trophoblast may be seen within the lumen in the spiral or uteroplacental arteries in the third trimester, when they would not normally be expected to be present then (Figure 3.18). This has been thought to reflect a teleological attempt to effect the physiological changes to ensure an adequate blood supply in the face of a compromised blood supply.19 The density of the interstitial trophoblast is reduced in preeclampsia, recapitulating the defect in miscarriage.
Placental origins of diabesity and the origin of preeclampsia
Published in Moshe Hod, Lois G. Jovanovic, Gian Carlo Di Renzo, Alberto de Leiva, Oded Langer, Textbook of Diabetes and Pregnancy, 2018
Gernot Desoye, Berthold Huppertz
However, a larger proportion of these maldeveloped placentas may also show defects in extravillous trophoblast development and hence may additionally result in impaired trophoblast invasion.105 In those cases, the villous syncytiotrophoblast is affected and releases factors by necrotic and aponecrotic shedding, while the maldevelopment of the extravillous trophoblast will alter maternal blood flow toward the placenta106 subsequently impairing fetal growth. Again, the overload of the maternal system will develop early in pregnancy (early-onset preeclampsia), growth of the fetus will be impaired as well (FGR), and changes in predictive angiogenic markers will be quite striking.107
Pre-eclampsia and non-proteinuric pregnancy-induced hypertension
Published in David M. Luesley, Mark D. Kilby, Obstetrics & Gynaecology, 2016
Although the primary events leading to preeclampsia are still unclear, it is now widely believed that a cascade of events leads to the clinical syndrome (summarised in Fig. 26.1). Although the inheritance of preeclampsia has yet to be characterised, there is a strong familial predisposition: a family history in either mother or sister increases the risk of preeclampsia four- to eight-fold. This genetic predisposition leads to a faulty interplay between the invading extravillous trophoblast cells (of fetal origin) and the maternal immunologically active decidual cells.
Regulatory roles of non-coding RNAs and m6A modification in trophoblast functions and the occurrence of its related adverse pregnancy outcomes
Published in Critical Reviews in Toxicology, 2022
Wang Rong, Wan Shukun, Wang Xiaoqing, Huang Wenxin, Dai Mengyuan, Mi Chenyang, Huidong Zhang
Female reproductive health is of great significance to the development of our society. Extravillous trophoblast (EVT) cells play an important role in embryonic development and healthy pregnancy. EVT cells can proliferate, migrate, invade into uterine decidua and reach decidual artery and uterine spiral artery (Ji et al. 2013; Abbas et al. 2020), which expands blood volume inside the uterus and placenta and also ensures better nutritional supply and endocrine immune environment for embryonic development (Lala and Nandi 2016). Dysfunctions of EVT cells might induce a serial of trophoblast-related adverse pregnancy outcomes, including PE (preeclampsia), GDM (gestational diabetes mellitus), FGR (fetal growth restriction), RM (recurrent miscarriage), stillbirth, premature birth, et al. (Khong et al. 1992; Norwitz 2006; Lash et al. 2010; Abbas et al. 2020), which might further induce morbidity and mortality for both mother and fetus (Rai and Regan 2006; Guo, Yang, et al. 2020).
Astaxanthin inhibiting oxidative stress damage of placental trophoblast cells in vitro
Published in Systems Biology in Reproductive Medicine, 2021
Jiu-Yuan Fu, Yang Jing, Yan-Ping Xiao, Xiao-Hua Wang, Yan-Wei Guo, Yan-Ju Zhu
The HTR-8 cell line is derived from normal human chorionic villus tissue and could be cultured and identified by histological culture methods. It has an invasive phenotype of extravillous trophoblast cell line. In order to achieve longer survival and increased the stability, the pS3-neo plasmid of the SV40 region upstream gene and the neomycin phosphotransferase gene were inserted into the HTR-8 cell line to establish the immortalized cell line HTR-8/SVneo (Abou-Kheir et al. 2017) that has been used in research about trophoblast-related diseases. The HTR-8/SVneo cells not only maintain the biological characteristics and phenotype like the original cells, but and high purity cultures are easy to prepare. HTR8/SVneo cells exposed to hypoxia/reoxygenation (H/R) revealed that oxidative stress from the trophoblasts is one of the possible pathological mechanisms of PE (Chen et al. 2016; Rao et al. 2019).
Human placental lactogen mRNA in maternal plasma play a role in prenatal diagnosis of abnormally invasive placenta: yes or no?
Published in Gynecological Endocrinology, 2019
Jing Li, Ning Zhang, Yan Zhang, Xiaoyu Hu, Guoqiang Gao, Yuanhua Ye, Wei Peng, Jun Zhou
The molecular mechanisms of increased hPL observed in women with invasive placenta are not clear. However, some investigators have proposed that the increased levels of hPL mRNA in maternal plasma of women with placenta accreta may be affected by direct uteroplacental transfer of placental mRNA molecules resulting from a connection between the placenta and maternal circulation and the presence of thin and dysfunctional decidua at the lower segment of the uterus [11,24]. Thus, the exact process by which placenta accreta is initiated is probably more complicated than just the abnormal decidualization of a scarred area or the lack of decidua in the lower uterine segment near the cervix. During placental formation, interstitial extravillous trophoblast cells are crucial for the invasion of the placenta into the uterine wall and may produce high levels of hPL [25]. Thus, we hypothesize that the increased levels of hPL in women who had invasive placenta observed in our study may reflect the activity of interstitial extravillous trophoblast.