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Project description:Trophoblast induced reprogramming of the decidualization program
| PRJNA812321 | ENA
Project description:The implanting embryo and developing placenta interface with the endometrium through a multinuclear trophoblast layer, syncytiotrophoblast (STB), which plays critical barrier, transport, immunomodulatory and endocrine roles throughout pregnancy. Understanding trophoblast and endometrial biology has recently been accelerated through sophisticated stem cell and organoid models, however few studies have combined these models to explore maternal-embryo communication. Here, we combined organoid models of secretory phase and decidual endometrial glands with trophoblast stem cell-derived STB to investigate signalling from maternal glands to the developing placenta. Luminal secretions collected from endometrial organoids by centrifugation were added to STB cultures and transcriptome analysis revealed that both secretory phase and decidual organoid secretions had profound effects on STB gene expression, inducing 3279 and 2634 differentially expressed genes (DEG), respectively (padj<0.05, >50% ≥1 log2 fold change). Gene set enrichment analysis of shared DEG (1926 genes) suggested upregulation of immune signalling and downregulation of mitochondrial respiration. Secretory and decidual secretions led to increased basal and maximal respiration (p<0.01) but reduced respiratory spare capacity (p<0.05) in STB, while glycolytic activity was also increased (p<0.05) together with increased expression of rate-limiting glycolysis enzymes HK1, HK2, PFKP and PKM (padj<0.03). Integrating cytokine array analysis of organoid secretions with upstream regulator analysis of STB DEG identified VEGFA and CSF1 as secretory products that might regulate mitochondrial and glycolytic genes, respectively, whereas secreted LCN2 and IL1A were upstream of immunomodulatory genes. Regulation of both immunomodulatory and metabolic gene sets was predicted for secreted CSF1 and EGF. The findings suggest that STB is highly responsive to endometrial gland secretions, which induce metabolic reprogramming likely to result in a more glycolytic phenotype in vivo as well as stimulating STB to modulate maternal immune responses. Endometrial gland signals thus shape trophoblast development to support successful establishment of pregnancy.
2025-11-30 | GSE308529 | GEO
Project description:Maternal-embryonic interactions play a critical role in successful pregnancy, with particular emphasis on the decidual-trophoblast interaction, which have been long recognized to exert a paracrine influence through the trophoblast cells on the progression of decidualization and the function of decidual cells. Despite this knowledge, the full extent of the embryo's impact on the decidua remains largely unexplored. To investigate the influence of embryonic signals on the maternal decidua, we utilized Prl3d1Cre/Cre mice mated with R26DTA/DTA mice, resulting in the generation of Prl3d1Cre/+, R26DTA/+ conceptus. In these conceptuses, the primary trophoblast giant cells (pTGCs) were selectively ablated by diphtheria toxin A (DTA). The pTGCs are the key embryonic cells that directly interact with the maternal decidua. Following the ablation of pTGCs, we observed impaired decidualization, as indicated by altered expression of genes related to decidualization or decidual function, such as Prl8a2, Wnt4, Bmp2, Alpl, and Hsd11b2, as well as a reduction in the interferon response in the decidua on day 6.5 of early pregnancy. Additionally, we found significant downregulation of numerous lipid-related biological effects in both deciduae on day 6.5 and day 8 of early pregnancy. These findings shed light on the complex interactions between the maternal and embryonic components during early pregnancy and underscore the importance of embryonic-derived influences on decidual lipid metabolism.
2024-11-30 | GSE240086 | GEO
Project description:During the invasive phase of implantation, trophoblasts and maternal decidual stromal cells secrete products that regulate trophoblast differentiation and migration into the maternal endometrium. Paracrine interactions between the extravillous trophoblast and the maternal decidua are important for successful embryonic implantation, including establishing the placental vasculature, anchoring the placenta to the uterine wall, and promoting immuno-acceptance of the fetal allograph. Global cross-talk between the trophoblast and the decidua has not been elucidated to date, and the current study used a functional genomics approach to investigate these paracrine interactions. Our data demonstrate a significant induction of pro-inflammatory cytokines and chemokines, as well as angiogenic/static factors in decidualized endometrial stromal cells in response to trophoblast-secreted products. The data suggest that the trophoblast acts to alter the local immune environment of the decidua to facilitate the process of implantation and assure an enriched cytokine/chemokine environment, while limiting mitotic activity of the stromal cells during the invasive phase of implantation. Keywords: Gene expression arrays in human stromal cells
2006-09-18 | GSE5809 | GEO
Project description:During the invasive phase of implantation, trophoblasts and maternal decidual stromal cells secrete products that regulate trophoblast differentiation and migration into the maternal endometrium. Paracrine interactions between the extravillous trophoblast and the maternal decidua are important for successful embryonic implantation, including establishing the placental vasculature, anchoring the placenta to the uterine wall, and promoting immuno-acceptance of the fetal allograph. Global cross-talk between the trophoblast and the decidua has not been elucidated to date, and the current study used a functional genomics approach to investigate these paracrine interactions. Human endometrial stromal cells were decidualized with progesterone and were further treated with conditioned media (CM) from human trophoblasts (TCM) or, as a control, with conditioned media (CCM) from non-decidualized stromal cells for 0, 3 and 12 hr. Total RNA was isolated and processed for analysis on whole genome, high density oligonucleotide arrays, containing 54,600 genes. Our data demonstrate a significant induction of pro-inflammatory cytokines and chemokines, as well as angiogenic/static factors in decidualized endometrial stromal cells in response to trophoblast-secreted products. The data suggest that the trophoblast acts to alter the local immune environment of the decidua to facilitate the process of implantation and assure an enriched cytokine/chemokine environment, while limiting mitotic activity of the stromal cells during the invasive phase of implantation.
2007-11-02 | E-GEOD-5809 | biostudies-arrayexpress
Project description:Decidual polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) are crucial for maternal–fetal stability and accumulate to support fetal development. Although advanced maternal age (AMA) increases the risk of adverse outcomes, the regulatory role and mechanism of decidual PMN-MDSCs in these outcomes remain unclear. Herein, the XCL1–XCR1 interaction mediated specific crosstalk between trophoblast cells and decidual PMN-MDSCs in both humans and mice. Single-cell sequencing identified a decidual PMN-MDSCs subset highly expressing XCR1 markedly reduced in AMA. Impaired XCL1-stimulated decidual XCR1+PMN-MDSCs delayed fetal growth in AMA and Xcr1-/- pregnant mice. Perinatal XCL1 supplementation and oltipraz treatment rescued these functions by activating decidual XCR1+PMN-MDSCs in AMA mice, not Xcr1-/- pregnant mice. The XCL1–XCR1 axis induced FOXO1 nuclear localization, regulating oxidative phosphorylation-related targets and enabling metabolic processes. Hence, XCL1–XCR1 crosstalk between trophoblast cells and PMN-MDSCs is critical in driving metabolic reprogramming of decidual XCR1+PMN-MDSCs and controlling adverse outcomes caused by AMA.
2026-04-08 | GSE289975 | GEO
Project description:Decidual polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) are crucial for maternal–fetal stability and accumulate to support fetal development. Although advanced maternal age (AMA) increases the risk of adverse outcomes, the regulatory role and mechanism of decidual PMN-MDSCs in these outcomes remain unclear. Herein, the XCL1–XCR1 interaction mediated specific crosstalk between trophoblast cells and decidual PMN-MDSCs in both humans and mice. Single-cell sequencing identified a decidual PMN-MDSCs subset highly expressing XCR1 markedly reduced in AMA. Impaired XCL1-stimulated decidual XCR1+PMN-MDSCs delayed fetal growth in AMA and Xcr1-/- pregnant mice. Perinatal XCL1 supplementation and oltipraz treatment rescued these functions by activating decidual XCR1+PMN-MDSCs in AMA mice, not Xcr1-/- pregnant mice. The XCL1–XCR1 axis induced FOXO1 nuclear localization, regulating oxidative phosphorylation-related targets and enabling metabolic processes. Hence, XCL1–XCR1 crosstalk between trophoblast cells and PMN-MDSCs is critical in driving metabolic reprogramming of decidual XCR1+PMN-MDSCs and controlling adverse outcomes caused by AMA.
2026-04-08 | GSE288405 | GEO
Project description:Decidual polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) are crucial for maternal–fetal stability and accumulate to support fetal development. Although advanced maternal age (AMA) increases the risk of adverse outcomes, the regulatory role and mechanism of decidual PMN-MDSCs in these outcomes remain unclear. Herein, the XCL1–XCR1 interaction mediated specific crosstalk between trophoblast cells and decidual PMN-MDSCs in both humans and mice. Single-cell sequencing identified a decidual PMN-MDSCs subset highly expressing XCR1 markedly reduced in AMA. Impaired XCL1-stimulated decidual XCR1+PMN-MDSCs delayed fetal growth in AMA and Xcr1-/- pregnant mice. Perinatal XCL1 supplementation and oltipraz treatment rescued these functions by activating decidual XCR1+PMN-MDSCs in AMA mice, not Xcr1-/- pregnant mice. The XCL1–XCR1 axis induced FOXO1 nuclear localization, regulating oxidative phosphorylation-related targets and enabling metabolic processes. Hence, XCL1–XCR1 crosstalk between trophoblast cells and PMN-MDSCs is critical in driving metabolic reprogramming of decidual XCR1+PMN-MDSCs and controlling adverse outcomes caused by AMA.
2026-04-08 | GSE288396 | GEO
Project description:Decidual natural killer cells promote extravillus trophoblast developmental pathways: evidence from trophoblast organoid co-cultures
| PRJNA1137979 | ENA
Project description:A Toxoplasma gondii infection during pregnancy can result in spontaneous abortion, preterm labor, or congenital fetal defects. The decidual immune system plays a critical role in regulating the immune micro-environment and in the induction of immune tolerance. To better understand the factors that mediate the decidual immune response associated with the T. gondii infection, a large-scale study employing TMT proteomics was conducted to characterize the differential decidual immune proteomes from infected and uninfected human decidual immune cells samples. The decidual immune cells from 105 human voluntary abortion tissues were purified, and of the 5510 unique proteins identified, 181 proteins were found to be differentially abundant (>1.2-fold cutoff, P＜0.05) in the T. gondii-infected decidual immune cells. 11 proteins of 181 differentially expressed proteins associated with trophoblast invasion, placental development, intrauterine fetal growth, and immune tolerance were verified using a quantitative real-time polymerase chain reaction and western blotting. This systematic research identified a broad range of immune factors in human decidual immune cells, shedding a new insight into the decidual immune molecular mechanism for abnormal pregnancy outcomes associated with T. gondii infection.
2018-07-27 | PXD008448 | Pride