O1. Dramatic upregulation of HIF-1α in the endovascular and extravillous trophoblasts at the maternal-fetal interface in preeclamptic pregnancies

2011 ◽  
Vol 1 (3-4) ◽  
pp. 257
Author(s):  
JongYun Hwang ◽  
Xiujun Fan ◽  
Joyce F. Sung ◽  
Sabita Dhal ◽  
Nihar R. Nayak ◽  
...  
Keyword(s):  
Extravillous Trophoblasts ◽  
Maternal Fetal Interface

scholarly journals The HLA-G cycle provides for both NK tolerance and immunity at the maternal–fetal interface

2015 ◽  
Vol 112 (43) ◽  
pp. 13312-13317 ◽  
Author(s):  
Tamara Tilburgs ◽  
J. Henry Evans ◽  
Ângela C. Crespo ◽  
Jack L. Strominger
Keyword(s):  
Natural Killer Cells ◽  
Confocal Microscopy ◽  
Virus Infection ◽  
Natural Killer ◽  
Stromal Cells ◽  
Synapse Formation ◽  
Initial Stage ◽  
Extravillous Trophoblasts ◽  
Maternal Fetal Interface ◽  
Decidual Natural Killer Cells

The interaction of noncytotoxic decidual natural killer cells (dNK) and extravillous trophoblasts (EVT) at the maternal–fetal interface was studied. Confocal microscopy revealed that many dNK interact with a single large EVT. Filamentous projections from EVT enriched in HLA-G were shown to contact dNK, and may represent the initial stage of synapse formation. As isolated, 2.5% of dNK contained surface HLA-G. However, surface HLA-G–negative dNK contained internalized HLA-G. Activation of dNK resulted in the disappearance of internalized HLA-G in parallel with restoration of cytotoxicity. Surface HLA-G was reacquired by incubation with EVT. This HLA-G cycle of trogocytosis, endocytosis, degradation, and finally reacquisition provides a transient and localized acquisition of new functional properties by dNK upon interaction with EVT. Interruption of the cycle by activation of dNK by cytokines and/or viral products serves to ensure the NK control of virus infection at the interface, and is illustrated here by the response of dNK to human cytomegalo virus (HCMV)-infected decidual stromal cells. Thus, the HLA-G cycle in dNK can provide both for NK tolerance and antiviral immunity.

scholarly journals HMGA1 Is a Potential Driver of Preeclampsia Pathogenesis by Interference with Extravillous Trophoblasts Invasion

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 822
Author(s):  
Keiichi Matsubara ◽  
Yuko Matsubara ◽  
Yuka Uchikura ◽  
Katsuko Takagi ◽  
Akiko Yano ◽  
...  
Keyword(s):  
Protein A ◽  
High Mobility ◽  
Extravillous Trophoblast ◽  
High Mobility Group Protein ◽  
Successful Pregnancy ◽  
Group Protein ◽  
Serious Disease ◽  
Proliferation And Invasion ◽  
Extravillous Trophoblasts ◽  
Fertilized Egg

Preeclampsia (PE) is a serious disease that can be fatal for the mother and fetus. The two-stage theory has been proposed as its cause, with the first stage comprising poor placentation associated with the failure of fertilized egg implantation. Successful implantation and placentation require maternal immunotolerance of the fertilized egg as a semi-allograft and appropriate extravillous trophoblast (EVT) invasion of the decidua and myometrium. The disturbance of EVT invasion during implantation in PE results in impaired spiral artery remodeling. PE is thought to be caused by hypoxia during remodeling failure–derived poor placentation, which results in chronic inflammation. High-mobility group protein A (HMGA) is involved in the growth and invasion of cancer cells and likely in the growth and invasion of trophoblasts. Its mechanism of action is associated with immunotolerance. Thus, HMGA is thought to play a pivotal role in successful pregnancy, and its dysfunction may be related to the pathogenesis of PE. The evaluation of HMGA function and its changes in PE might confirm that it is a reliable biomarker of PE and provide prospects for PE treatment through the induction of EVT proliferation and invasion during the implantation.

scholarly journals Low chorionic villous succinate accumulation associates with recurrent spontaneous abortion risk

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Xiao-Hui Wang ◽  
Sha Xu ◽  
Xiang-Yu Zhou ◽  
Rui Zhao ◽  
Yan Lin ◽  
...  
Keyword(s):  
Spontaneous Abortion ◽  
Embryo Implantation ◽  
Underlying Mechanism ◽  
Recurrent Spontaneous Abortion ◽  
Extravillous Trophoblast ◽  
Trophoblast Invasion ◽  
Iron Sulfur ◽  
Succinate Dehydrogenase Complex ◽  
Extravillous Trophoblasts ◽  
Control Study

AbstractDysregulated extravillous trophoblast invasion and proliferation are known to increase the risk of recurrent spontaneous abortion (RSA); however, the underlying mechanism remains unclear. Herein, in our retrospective observational case-control study we show that villous samples from RSA patients, compared to healthy controls, display reduced succinate dehydrogenase complex iron sulfur subunit (SDHB) DNA methylation, elevated SDHB expression, and reduced succinate levels, indicating that low succinate levels correlate with RSA. Moreover, we find high succinate levels in early pregnant women are correlated with successful embryo implantation. SDHB promoter methylation recruited MBD1 and excluded c-Fos, inactivating SDHB expression and causing intracellular succinate accumulation which mimicked hypoxia in extravillous trophoblasts cell lines JEG3 and HTR8 via the PHD2-VHL-HIF-1α pathway; however, low succinate levels reversed this effect and increased the risk of abortion in mouse model. This study reveals that abnormal metabolite levels inhibit extravillous trophoblast function and highlights an approach for RSA intervention.

Kisspeptin/Kiss1r system and angiogenic and immunological mediators at the maternal-fetal interface of domestic cats

2021 ◽  
Author(s):  
Luciano Cardoso Santos ◽  
Jeane Martinha dos Anjos Cordeiro ◽  
Larissa da Silva Santana ◽  
Bianca Reis Santos ◽  
Erikles Macêdo Barbosa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Late Pregnancy ◽  
Domestic Cats ◽  
Placental Angiogenesis ◽  
Spatiotemporal Expression ◽  
Gene Correlation ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Maternal Fetal Interface

Abstract The Kisspeptin/Kiss1r system is a key regulator of reproduction by stimulating gonadotrophin-releasing hormone (GnRH) and luteinizing hormone (LH) release, and in vitro studies have shown that Kisspeptin can modulate angiogenesis and immune function, factors that are also essential for reproduction However, there are no studies on the expression of Kisspeptin/Kiss1r at the maternal-fetal interface in domestic cats and its relationship with angiogenic and immunological mediators. Thus, our objective was to evaluate the spatiotemporal expression profile of Kisspeptin/Kiss1r and angiogenic and immunological mediators in the uterus and placenta of domestic cats during pregnancy. Uterus and placenta samples were collected from cats in mid pregnancy (N = 6) and late pregnancy (N = 6), in addition to uterus from non-pregnant cats in diestrus (N = 7), to evaluate protein and gene expression of Kiss1, Kiss1r, VEGF, Flk-1, PLGF, INFγ, MIF, TNFα, IL6, and IL10 by immunohistochemistry and qPCR. Pregnancy increased the uterine expression of Kiss1 and Kiss1r, especially at the late pregnancy, in addition to upregulating INFy, MIF, Vegf, Il10, and Tnf and downregulating Plgf. Higher placental expression of Kiss1r and Plgf mRNA occurred at the late pregnancy, while the expression of Kiss1, VEGF, Flk-1, INFy, TNFα, Il6, and IL10 was higher in the mid of pregnancy. A positive correlation between Kiss1 and Tnf was observed in the placenta, while Kiss1r had a negative correlation with Infγ, Il6, and Il10. The findings reveal that Kisspeptin/Kiss1r and angiogenic and immunological mediators at the maternal-fetal interface of pregnant cat have a gene correlation and are modulated by the gestational age. These data suggest possible functional links of Kisspeptin in placental angiogenesis and immunology.

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