Decidualized endometrial stromal cell derived factors promote trophoblast invasion

Godbole, Geeta; Suman, Pankaj; Gupta, Seema; Modi, Deepak

doi:10.1016/j.fertnstert.2010.09.045

Cited by 77 publications

(62 citation statements)

References 33 publications

(44 reference statements)

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“…We observed a time-dependent increased expression of these three markers (between D3 and D15), in the presence of the differentiation medium, indicating that ESCs are fully differentiated at D15. This result is commonly observed for in vitro ESC decidualization in the presence of E2 and P4 (Kasahara et al 2001, Godbole et al 2011. We also studied adiponectin effect on ESC decidualization.…”

Section: Discussionsupporting

confidence: 64%

“…As one of the major roles of decidual cells is the control of trophoblast invasion (Godbole et al 2011, Sharma et al 2016, we next looked at whether adiponectin could modify the ability of decidualized ESCs to regulate this process. Therefore, we used Transwell assays to estimate the trophoblast HTR-8/SVneo cell line invasive capacities when seeded with CM from ESCs treated or not with adiponectin.…”

Section: Discussionmentioning

confidence: 99%

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Adiponectin limits differentiation and trophoblast invasion in human endometrial cells

Duval

Santos

Moindjie

et al. 2017

Journal of Molecular Endocrinology

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Successful human embryo implantation requires a proper differentiation of endometrial stromal cells (ESCs) into decidual cells, during a process called decidualization. ESCs express specific molecules, such as prolactin, insulin-like growth factor-binding protein-1 (IGFBP-1) and connexin-43. Decidual cells are also involved in the control of trophoblast invasion, by secreting various factors, such as matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). Adiponectin is an adipokine with insulin-sensitizing, anti-inflammatory and anti-proliferative effects. At the embryomaternal interface, adiponectin promotes differentiation and invasion of human trophoblastic cells. We hypothesize that the effects of adiponectin on endometrium could counteract its pro-invasive effects previously described in the human trophoblast. In this context, we have firstly demonstrated that adiponectin downregulates IGFBP-1 and connexin-43 mRNA expressions, as well as prolactin secretion in ESCs, suggesting an anti-differentiative effect of adiponectin. Secondly, we found that invasive capacities of trophoblastic cell line HTR-8/SVneo are reduced in the presence of conditioned media from ESC cultured in the presence of adiponectin. Adiponectin's anti-invasive action is associated with a decreased activity of MMP-2 and MMP-9, and an increased TIMP-3 mRNA expression in ESCs. Finally, adiponectin receptors (ADIPOR1 and ADIPOR2) knockdown abolishes the anti-differentiative and anti-invasive effects of adiponectin in human ESCs. Altogether, our results suggest that adiponectin reduces the decidualization process and inversely induces the production of endometrial factors that limit trophoblast invasion. Thus, through a dual control in trophoblast and endometrial cells, adiponectin appears as a pivotal actor of the embryo implantation process.

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Section: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Adiponectin limits differentiation and trophoblast invasion in human endometrial cells

Duval

Santos

Moindjie

et al. 2017

Journal of Molecular Endocrinology

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“…Chemokines regulate the main events that occurred at the maternal-fetal interface, such as the endometrium decidualization, vessel remodeling and immune tolerance (Kuang et al 2009, Godbole et al 2011. Moreover, chemokines were also proven to modulate the biological functions of trophoblasts, and finally regulate the process of embryo implantation.…”

Section: Discussionmentioning

confidence: 99%

Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy

Meng

Shang

et al. 2015

Reproduction

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Chemokine CCL24, acting through receptor CCR3, is a potent chemoattractant for eosinophil in allergic diseases and parasitic infections. We recently reported that CCL24 and CCR3 are co-expressed by trophoblasts in human early pregnant uterus. Here we prove with evidence that steroid hormones estradiol (E), progesterone (P), and human chorionic gonadotropin (hCG), as well as decidual stromal cells (DSCs) could regulate the expression of CCL24 and CCR3 of trophoblasts. We further investigate how trophoblast-derived CCL24 mediates the function of trophoblasts in vitro, and conclude that CCL24/CCR3 promotes the proliferation, viability and invasiveness of trophoblasts. In addition, analysis of the downstream signaling pathways of CCL24/CCR3 show that extracellular signal-regulated kinases (ERK1/2) and phosphoinositide 3-kinase (PI3K) pathways may contribute to the proliferation, viability and invasiveness of trophoblasts by activating intracellular molecules Ki67 and matrix metallopeptidase 9 (MMP9). However, we did not observe any inhibitory effect on trophoblasts when blocking c-Jun N-terminal kinase (JNK) or p38 pathways. In conclusion, our data suggests that trophoblast-derived CCL24 at the maternal-fetal interface promotes trophoblasts cell growth and invasiveness by ERK1/2 and PI3K pathways. Meanwhile, pregnancy-related hormones (P and hCG), as well as DSCs could up-regulate CCL24/CCR3 expression in trophoblasts, which may indirectly influence the biological functions of trophoblasts. Thus, our results provide a possible explanation for the growth and invasion of trophoblasts in human embryo implantation. Reproduction (2015) 150 417-427

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“…In addition to forming a maternal barrier against invasive trophoblast, decidualization has been suggested to actively control trophoblasts. For example, the invasiveness and growth of cultured trophoblast cells is decreased in conditioned medium from decidual cells (Lewis et al 1993;Zhu et al 2009;Godbole et al 2011). Decidual effects are not uniformly suppressive; rather they involve fine-tuned interactions via numerous pathways (Knofler 2010).…”

Section: [Supplemental Materials Is Available For This Article]mentioning

confidence: 99%

Single-cell transcriptomics of the human placenta: inferring the cell communication network of the maternal-fetal interface

et al. 2017

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Organismal function is, to a great extent, determined by interactions among their fundamental building blocks, the cells. In this work, we studied the cell-cell interactome of fetal placental trophoblast cells and maternal endometrial stromal cells, using single-cell transcriptomics. The placental interface mediates the interaction between two semiallogenic individuals, the mother and the fetus, and is thus the epitome of cell interactions. To study these, we inferred the cell-cell interactome by assessing the gene expression of receptor-ligand pairs across cell types. We find a highly cell-type-specific expression of G-protein-coupled receptors, implying that ligand-receptor profiles could be a reliable tool for cell type identification. Furthermore, we find that uterine decidual cells represent a cell-cell interaction hub with a large number of potential incoming and outgoing signals. Decidual cells differentiate from their precursors, the endometrial stromal fibroblasts, during uterine preparation for pregnancy. We show that decidualization (even in vitro) enhances the ability to communicate with the fetus, as most of the receptors and ligands up-regulated during decidualization have their counterpart expressed in trophoblast cells. Among the signals transmitted, growth factors and immune signals dominate, and suggest a delicate balance of enhancing and suppressive signals. Finally, this study provides a rich resource of gene expression profiles of term intravillous and extravillous trophoblasts, including the transcriptome of the multinucleated syncytiotrophoblast.

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Decidualized endometrial stromal cell derived factors promote trophoblast invasion

Cited by 77 publications

References 33 publications

Adiponectin limits differentiation and trophoblast invasion in human endometrial cells

Adiponectin limits differentiation and trophoblast invasion in human endometrial cells

Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy

Single-cell transcriptomics of the human placenta: inferring the cell communication network of the maternal-fetal interface

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