scholarly journals Human chorionic gonadotropin (hCG) modulation of TIMP1 secretion by human endometrial stromal cells facilitates extravillous trophoblast invasion in vitro

2013 ◽  
Vol 28 (8) ◽  
pp. 2215-2227 ◽  
Author(s):  
A. Tapia-Pizarro ◽  
F. Argandona ◽  
W. A. Palomino ◽  
L. Devoto
Keyword(s):  
Chorionic Gonadotropin ◽  
Human Chorionic Gonadotropin ◽  
Stromal Cells ◽  
Extravillous Trophoblast ◽  
Trophoblast Invasion ◽  
Endometrial Stromal Cells

Human chorionic gonadotropin improves endometrial receptivity by increasing the expression of homeobox A10

2020 ◽  
Vol 26 (6) ◽  
pp. 413-424
Author(s):  
Mengchen Zhu ◽  
Shanling Yi ◽  
Xiaomin Huang ◽  
Junan Meng ◽  
Haixiang Sun ◽  
...  
Keyword(s):  
Chorionic Gonadotropin ◽  
Human Chorionic Gonadotropin ◽  
Embryo Implantation ◽  
Endometrial Receptivity ◽  
Endometrial Stromal Cells ◽  
Healthy Control ◽  
Hcg Receptor ◽  
Methyltransferase 1

Abstract Homeobox A10 (HOXA10) is a characterized marker of endometrial receptivity. The mechanism by which hCG intrauterine infusion promotes embryo implantation is still unclear. This study seeks to investigate whether hCG improves endometrial receptivity by increasing expression of HOXA10. HOXA10 expression with human chorionic gonadotropin stimulation was analyzed in vitro and in vivo. Our results demonstrate that HOXA10 was decreased in the endometria of recurrent implantation failure patients compared to that in the healthy control fertile group, also we observed that hCG intrauterine infusion increased endometrial HOXA10 expression. HOXA10, blastocyst-like spheroid expansion area was increased, whereas DNA (cytosine-5-)-methyltransferase 1 was decreased when human endometrial stromal cells (hESCs) were treated with 0.2 IU/ml of hCG for 48 h. HOXA10 promoter methylation was also reduced after hCG treatment. Collagen XV (ColXV) can repress the expression of DNA (cytosine-5-)-methyltransferase 1, and hCG treatment increased the expression of ColXV. However, when the hESCs were treated with LH/hCG receptor small interfering RNA to knock down LH/hCG receptor, hCG treatment failed to repress DNA (cytosine-5-)-methyltransferase 1 expression or to increase ColXV expression. Our findings suggest that hCG may promote embryo implantation by increasing the expression of HOXA10.

scholarly journals Human Endometrial Stromal Cells Are Highly Permissive To Productive Infection by Zika Virus

2016 ◽  
Author(s):  
Isabel Pagani ◽  
Silvia Ghezzi ◽  
Adele Ulisse ◽  
Alicia Rubio ◽  
Filippo Turrini ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Zika Virus ◽  
Female Reproductive Tract ◽  
Productive Infection ◽  
Trophoblast Invasion ◽  
Societal Implications ◽  
Zikv Infection ◽  
Endometrial Stromal Cells ◽  
First Time

ABSTRACTZika virus (ZIKV) is a recently re-emerged flavivirus transmitted to humans by mosquito bites but also from mother to fetus and by sexual intercourse. We here show for the first time that primary human endometrial stromal cells (HESC) are highly permissive to ZIKV infection and support its in vitro replication. ZIKV envelope expression was detected in the endoplasmic reticulum whereas double-stranded viral RNA colocalized with vimentin filaments to the perinuclear region. ZIKV productive infection also occurred in the human T-HESC cell line with the induction of interferon-β (IFN-β) and of IFN-stimulated genes. Notably, in vitro decidualization of T-HESC with cyclic AMP and progesterone upregulated the cell surface expression of the ZIKV entry co-receptor AXL and boosted ZIKV replication by ca. 100-fold. Thus, endometrial stromal cells, particularly if decidualized, likely represent a crucial cell target of sexual virus transmission and a relevant source of ZIKV spreading to placental trophoblasts during pregnancy.AUTHOR SUMMARYInfection by Zika virus (ZIKV), a flavivirus transmitted to humans by mosquito bites, has recently emerged as an important cause of neurological lesions in the fetal brain as women who become infected by ZIKV during pregnancy can transmit the virus to their fetus. In addition, routes of ZIKV transmission independent of mosquito bites have been also identified and include sexual transmission from both infected men and women to their partners, an aspect bearing great societal implications for ZIKV spread. These observations highlight the importance of the female reproductive tract in the establishment and/or spreading of the infection. In this regard, the endometrium is a highly dynamic tissue undergoing major histological changes during the menstrual cycle under the coordinated action of sexual hormones. In particular, progesterone drives the differentiation of human endometrial stromal cells towards decidualization, a process that is critical for fetal trophoblast invasion and placenta formation. We here report for the first time that both primary and immortalized human endometrial stromal cells are highly permissive to ZIKV infection and replication, particularly when in vitro decidualized by progesterone, suggesting that these cells could significantly contribute to vertical ZIKV transmission in utero during pregnancy but also to horizontal transmission by the sexual route.

scholarly journals Human Chorionic Gonadotropin Produced by the Invasive Trophoblast But Not the Villous Trophoblast Promotes Cell Invasion and Is Down-Regulated by Peroxisome Proliferator-Activated Receptor-γ

Endocrinology ◽  
2007 ◽  
Vol 148 (10) ◽  
pp. 5011-5019 ◽  
Author(s):  
Karen Handschuh ◽  
Jean Guibourdenche ◽  
Vassilis Tsatsaris ◽  
Mickaël Guesnon ◽  
Ingrid Laurendeau ◽  
...  
Keyword(s):  
Chorionic Gonadotropin ◽  
Cell Invasion ◽  
Human Chorionic Gonadotropin ◽  
Primary Cultures ◽  
Trophoblast Invasion ◽  
Peroxisome Proliferator ◽  
Dependent Manner ◽  
Peroxisome Proliferator Activated Receptor ◽  
Villous Trophoblast

A critical step in the establishment of human pregnancy is the invasion of the uterus wall by extravillous cytotrophoblasts (EVCTs) during the first trimester. It is well established that human chorionic gonadotropin hormone (hCG) is secreted by the endocrine syncytiotrophoblast (ST) into the maternal compartment. We recently reported that invasive EVCTs also produce hCG, suggesting an autocrine role in the modulation of trophoblast invasion. Here we analyzed the role of hCG secreted in vitro by primary cultures of invasive EVCT and noninvasive ST. We first demonstrated that LH/CG receptor was present in EVCTs in situ and in vitro as well as in an EVCT cell line (HIPEC65). We next showed that hCG secreted by EVCTs stimulated progesterone secretion by MA10 cells in a concentration-dependent manner. Incubation of HIPEC65 with EVCT supernatants induced a 10-fold increase in cell invasion, whereas ST supernatants had no effect. This stimulating effect was strongly decreased when hCG was depleted from EVCT supernatants containing a large amount of the hyperglycosylated form of hCG, which is almost undetectable in ST supernatants. Finally, we investigated the regulation of hCG expression by peroxisome proliferator-activated receptor (PPAR)-γ, a nuclear receptor shown to inhibit trophoblast invasion. Activation of PPARγ decreased α- and β-subunit transcript levels and total hCG secretion in primary EVCTs. Our results offer the first evidence that hCG secreted by the invasive trophoblast, likely the hyperglycosylated form of hCG, but not by the syncytiotrophoblast, promotes trophoblast invasion and may be a PPARγ target gene in trophoblast invasion process.

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