Effects of dPRP (PRL8a2) on gene expression of decidual-placental-embryonic tissue
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ABSTRACT: DPRP (PRL8a2) is critically involved in adaptations of the placentation site to physiological stressors. DPRP (PRL8a2) restrains the expression of genes associated with ER stress. We used DNA microarrays to analyze the transcriptome of wild type and dPRP null mouse decidual-placental-embryonic tissues from gestation day 7.5.
Project description:DPRP (PRL8a2) is critically involved in adaptations of the placentation site to physiological stressors. DPRP (PRL8a2) restrains the expression of genes associated with ER stress.
Project description:To understand the regulation of cytotoxicity by decidual CD8+ T cells (CD8+ dT) at the maternal-fetal interface, gene expression analysis of CCR7-CD45RA- effector-memory CD8+ T cells isolated from peripheral blood of unrelated healthy controls and decidual tissue from first trimester (6-12 weeks) and term (>37 weeks) pregnancy was performed. Furthermore, first trimester decidual effector-memory CD8+ T cells were stimulated with anti-CD3/CD28 in the presence of IL-2 for 12 hours or 72 hours. RNA was isolated and gene expression profiles were generated by employing Affymetrix HG_U133_Plus 2 arrays on the Affymetrix Geneatlas system.
Project description:In the present study, to better define the aspects of decidual cell polyploidy, we isolated pure polyploid and non-polyploid decidual cell populations from the in vivo decidual bed. Three independent RNA pools prepared for each population were then subjected to the Affymetrix gene chip analysis for the whole mouse genome transcripts. Our data revealed up-regulation of 1015 genes and down-regulation of 1207 genes in the polyploid populations, as compared to the non-polyploid group. We analyzed whole gnenome transcription from non-polyploid and polyploid cell populations using the Affymetrix GeneChip® Mouse Gene 1.0 ST Array . 3 replicates were performed.
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.
Project description:Decidual macrophage populations, CD11cHI and CD11cLO cells were analyzed for expression profiles and unique characteristics. We used microarrays to detail the global program of gene expression and to determine differences between these two unique decidual macrophage populations. First trimester decidual tissue was digested in order to release immune cells. Cells were stained for CD14 and CD11c and purified by MoFlo sorting. Cells were immediately lysed for RNA extraction and hybridization on Affymetrix microarrays. We utilized 8 patient paired samples (total of 16 microarrays).
Project description:We used full genome microarrays to profile the full lifetime of the mouse placenta from embryonic day 8.5 (e8.5), at the time of chorioallantoic fusion, until postnatal day 0 (P0). At each stage, the fetal placenta and maternal decidual tissues were dissected and profiled separately Experiment Overall Design: Mouse placentas were obtained from timed pregnant female mice at each timepoint, and fetal tissues were used to confirm embryo staging. Fetal placenta and maternal decidual tissues were dissected and pooled separately for each litter prior to RNA extraction and hybridization on Affymetrix microarrays.
Project description:Natural killer cells (NKs) are abundant in the human decidua. Several diseases of poor placental development are associated with first pregnancies, and we thus looked to characterize differences in decidual NKs in first versus repeated pregnancies. We discovered a population unique to repeated pregnancies, which possesses a novel transcriptome and epigenetic signature, characterized with high expression levels of the receptors NKG2C and LILRB1. Activation of these receptors leads to increased production and secretion of IFNγ and VEGFa, the latter found to support vascular sprouting and trophoblast-tumor growth. We propose that this population represents NK “memory” of pregnancy, and have named these cells Pregnancy Trained decidual NK cells (PTdNKs). We further suggest that the precursors of PTdNKs are found in the endometrium. PTdNKs may prove useful in understanding and treating disorders of poor placentation.
Project description:We used full genome microarrays to profile the full lifetime of the mouse placenta from embryonic day 8.5 (e8.5), at the time of chorioallantoic fusion, until postnatal day 0 (P0). For these samples, at each stage the fetal placenta and maternal decidual tissues were dissected and profiled separately (See series 1). For this experiment (Series 2), placental and decidual timecourse samples were normalized and modeled with two undissected (including placental and decidual tissue) e17 placentas to allow for scaling of values for comparison to the undissected placenta samples used in the publicly available mouse GeneAtlas dataset Keywords: time course
Project description:Placentation differs in the BN rat strain when compared to HSD and DSS rat strains. Intrauterine trophoblast invasion is shallow and the junctional zone is underdeveloped in the BN rat. These structural differences are striking but their quantification is not conducive to high throughput analyses. In the rat, the junctional zone can be readily dissected and is more homogenous than other components of the placentation site. HSD and BN rat gestation day 18.5 junctional zone gene expression profiles were determined using DNA microarray analysis to identity placenta-associate quantitate traits. Total RNAs from Junctional zone tissues of gestation day18.5 HSD and BN rat strains were subjected to microarray analyses. Three biological replicates of each strains were analyzed.
Project description:Macrophages are abundant in uterine mucosa during the peri-implantation phase and early pregnancy. Decidual macrophages display dynamic changes alone with pregnancy progress: During the peri-implantation phase, macrophages displayed a pro-inflammatory phenotype which facilitates embryo implantation. While, In the late firster trimester and second trimester, decidual macrophages are anti-proinflammatory which are helpful to pregnancy maintenance. Alterations in the ratio of pro-inflammatory/anti-inflammatory decidual macrophages lead to abortion, preeclampsia, and preterm birth. Placenta-derived exosomes (pEXO) are critical in the immune cell modulation such as T cell apoptosis, NK activities, and T regulatory (Treg) differentiation. However, it is unknown whether placenta-derived exosomes contribute to decidual macrophage polarization during early pregnancy. Here we report that exosomes from the placenta explant stimulate M2 macrophage polarization via exosomal miRNA-30d-5p. Mechanistically, miRNA-30d-5p polarized macrophages to M2 phenotype by inhibiting HDAC9 expression. Furthermore, the conditioned medium of pEXO-treated macrophages promoted trophoblast migration and invasion. By contrast, conditioned medium impaired the ability of endothelial cell tube formation. However, pEXO-treated macrophages have no impact on T cell proliferation. Together, we demonstrated that pEXO promoted trophoblast migration and invasion, endothelial cell migration, and attenuation of endothelial cell tube formation by polarizing macrophage to decidua-like macrophage.