Transcription profiling of human chorionic villi cells co-culutured with fetal cardiomyocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Akihiro Umezawa
PROVIDER: E-GEOD-7021 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:In the chorionic villi of placenta, trophoblasts and endothelial cells are present, and moreover mesenchymal cells (stromal cells) can be obtained. We generated cells with the mesenchymal phenotype from the chorionic mesoderm, and showed that: a) physiologically functioning cardiomyocytes were transdifferentiated from human placenta-derived chorionic villi cells, but these cells did not induce to osteoblasts and adipocytes ; b) the cardiomyogenic induction rate obtained using our system was relatively high compared to that obtained using the previously described method ; c) co-cultivation with fetal murine cardiomyocytes alone without transdifferentiation factors such as 5-azaC or oxytocin is sufficient for cardiomyogenesis in our system; d) Chorionic villi cells have the electrophysiological properties of 'working' cardiomyocytes. The chorionic mesoderm contained a large number of cells with a cardiomyogenic potential. Keywords: Cardiomyogenic induction
2007-02-17 | GSE7021 | GEO
Project description:The placenta is considered one of the candidate cell sources in cellular therapeutics because of a large number of cells and heterogenous cell population with myogenic potentials. We first analyzed myogenic potential of cells obtained from six parts of the placenta, i.e., umbilical cord, amniotic epithelium, amniotic mesoderm, chorionic plate, villous chorion (chorion frondosum), , and decidua basalis. Implantation of placenta-derived cells into dystrophic muscles of immunodeficient mdx mice restored sarcolemmal expression of human dystrophin. Co-existence of human and murine nuclei in one myotube and presence of human dystrophin in murine myotube suggests that human dystrophin expression is due to cell fusion between host murine myocytes and implanted human cells. In vitro analysis revealed that cells derived from amniotic mesoderm, chorionic plate, ,and villous chorion efficiently transdifferentiate into myotubes. These cells fused to C2C12 murine myoblasts by in vitro co-culturing, and murine myoblasts start to express human dystrophin after fusion. These results demonstrate that placenta-derived cells, especially extraembryonic mesodermal cells, have a myogenic potential and regenerative capacity of skeletal muscle. Determination of cell specification with the gene chip analysis revealed that each placental cell has a distinct expression pattern. Experiment Overall Design: To isolate chorionic villi cells, we used the explant culture method, in which the cells were outgrown from pieces of chorionic villi attached to dishes. Chorionic villi cells were harvested with 0.25% trypsin and 1 mM EDTA, and overlaid onto the cultured fetal cardiomyocytes at 7 x 103/cm2. Every 2 days, the culture medium was replaced with fresh culture medium that was supplemented with 10% FBS and 1 ug/ml Amphotericin B (GIBCO). The morphology of the beating chorionic villi cells was evaluated under a fluorescent microscope.
2008-06-20 | E-GEOD-11510 | biostudies-arrayexpress
Project description:Placental trophoblasts are key determinants of in utero development. Mouse trophoblast stem cells (mTSCs), which were first derived over a decade ago, are a powerful cell culture model for studying their self-renewal or differentiation. Our attempts to isolate an equivalent population from the trophectoderm of human blastocysts generated colonies that quickly differentiated in vitro. This finding suggested that the human placenta has another progenitor niche. Here we show that the chorion is one such site. Initially, we immunolocalized pluripotency factors and trophoblast fate determinants in the early-gestation placenta, amnion and chorion. Immunoreactive cells were numerous in the chorion. We isolated these cells and plated them in medium containing FGF and an inhibitor of activin/nodal signaling, which is required for human embryonic SC self-renewal. Colonies of polarized cells with a limited lifespan emerged. Trypsin dissociation yielded continuously self-replicating monolayers. Colonies and monolayers formed the two major human trophoblast lineages—multinucleate syncytiotrophoblasts and invasive cytotrophoblasts (CTBs). Transcriptional profiling experiments revealed the factors associated with the self-renewal or differentiation of human chorionic trophoblast progenitor cells (TBPCs). They included imprinted genes, NR2F1/2, HMGA2 and adhesion molecules that were required for TBPC differentiation. Together, the results of these experiments suggested that the chorion is one source of epithelial CTB progenitors. These findings explain why CTBs of fully formed chorionic villi have a modest mitotic index and identify the chorionic mesoderm as a niche for TBPCs that support placental growth. TBPC colonies (3 biological replicates), TPBC monolayers (2 biological replicates), CTB (3 biological replicates), hESC (3 biological replicates)
2011-06-22 | E-GEOD-30127 | biostudies-arrayexpress
Project description:Placental trophoblasts are key determinants of in utero development. Mouse trophoblast stem cells (mTSCs), which were first derived over a decade ago, are a powerful cell culture model for studying their self-renewal or differentiation. Our attempts to isolate an equivalent population from the trophectoderm of human blastocysts generated colonies that quickly differentiated in vitro. This finding suggested that the human placenta has another progenitor niche. Here we show that the chorion is one such site. Initially, we immunolocalized pluripotency factors and trophoblast fate determinants in the early-gestation placenta, amnion and chorion. Immunoreactive cells were numerous in the chorion. We isolated these cells and plated them in medium containing FGF and an inhibitor of activin/nodal signaling, which is required for human embryonic SC self-renewal. Colonies of polarized cells with a limited lifespan emerged. Trypsin dissociation yielded continuously self-replicating monolayers. Colonies and monolayers formed the two major human trophoblast lineages—multinucleate syncytiotrophoblasts and invasive cytotrophoblasts (CTBs). Transcriptional profiling experiments revealed the factors associated with the self-renewal or differentiation of human chorionic trophoblast progenitor cells (TBPCs). They included imprinted genes, NR2F1/2, HMGA2 and adhesion molecules that were required for TBPC differentiation. Together, the results of these experiments suggested that the chorion is one source of epithelial CTB progenitors. These findings explain why CTBs of fully formed chorionic villi have a modest mitotic index and identify the chorionic mesoderm as a niche for TBPCs that support placental growth.
2011-06-22 | GSE30127 | GEO
Project description:The placenta is considered one of the candidate cell sources in cellular therapeutics because of a large number of cells and heterogenous cell population with myogenic potentials. We first analyzed myogenic potential of cells obtained from six parts of the placenta, i.e., umbilical cord, amniotic epithelium, amniotic mesoderm, chorionic plate, villous chorion (chorion frondosum), , and decidua basalis. Implantation of placenta-derived cells into dystrophic muscles of immunodeficient mdx mice restored sarcolemmal expression of human dystrophin. Co-existence of human and murine nuclei in one myotube and presence of human dystrophin in murine myotube suggests that human dystrophin expression is due to cell fusion between host murine myocytes and implanted human cells. In vitro analysis revealed that cells derived from amniotic mesoderm, chorionic plate, ,and villous chorion efficiently transdifferentiate into myotubes. These cells fused to C2C12 murine myoblasts by in vitro co-culturing, and murine myoblasts start to express human dystrophin after fusion. These results demonstrate that placenta-derived cells, especially extraembryonic mesodermal cells, have a myogenic potential and regenerative capacity of skeletal muscle. Determination of cell specification with the gene chip analysis revealed that each placental cell has a distinct expression pattern. Keywords: Determination of cell specification
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Project description:Pregnancy loss is often caused by chromosomal abnormalities of the conceptus. The prevalence of these abnormalities and the allocation of (ab)normal cells in embryonic and placental lineages during intrauterine development remain elusive. We analyzed 1,745 spontaneous pregnancy losses and found that roughly half (50.4%) of the products of conception (POC) were karyotypically abnormal, with maternal and paternal age independently contributing to the increased genomic aberration rate in pregnancy loss. We applied genome haplarithmisis to a subset of 94 pregnancy losses with normal parental and POC karyotypes. Genotyping of parental DNA as well as POC extraembryonic mesoderm and chorionic villi DNA, representing embryonic and trophoblastic tissues, enabled characterization of the genomic landscape of both lineages. Of these pregnancy losses, 35.1% had chromosomal aberrations not previously detected by karyotyping, increasing the rate of aberrations of pregnancy losses to 67.8% by extrapolation. In contrast to viable pregnancies where mosaic chromosomal abnormalities are often restricted to chorionic villi, such as confined placental mosaicism, we found a higher degree of mosaic chromosomal imbalances in extraembryonic mesoderm rather than chorionic villi in pregnancy losses. Our results stress the importance of scrutinizing the full allelic architecture of genomic abnormalities in pregnancy loss to improve clinical management and basic research of this devastating condition.
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Project description:In the bovine placenta, intimate fetomaternal contacts are confined to multiple discrete structures termed placentomes. In the placentomes, widely ramified fetal chorionic villi interdigitate with corresponding maternal caruncular crypts. The trophoblast covering the chorionic villi is composed of uninucleate trophoblast cells (UTCs) and binucleate trophoblast giant cells (TGCs). TGCs are weakly invasive and capable of migrating toward the caruncular epithelium where they eventually fuse with single epithelial cells to form short-living trinucleate fetomaternal hybrid cells. Thereby, molecules of fetal origin are transported into the maternal compartment. The loss of TGCs due to fetomaternal hybrid cell formation is compensated by differentiation of UTCs into TGCs. We performed a genome-wide gene expression study of virtually pure UTCs and TGCs to to identify genes which are associated with trophoblast cell differentiation
2019-12-31 | GSE122474 | GEO
Project description:VEGFR2 (Vascular endothelial growth factor receptor 2) is a central regulator of placental angiogenesis. The study of the VEGFR2 proteome of chorionic villi at term revealed its partners MDMX (Double minute 4 protein) and PICALM (Phosphatidylinositol-binding clathrin assembly protein). Subsequently, the oxytocin receptor (OT-R) and vasopressin V1aR receptor were detected in MDMX and PICALM immunoprecipitations. Immunogold electron microscopy showed VEGFR2 on endothelial cell (EC) nuclei, mitochondria, and Hofbauer cells (HC), tissue-resident macrophages of the placenta. MDMX, PICALM, and V1aR were located on EC plasma membranes, nuclei, and HC nuclei. Unexpectedly, PICALM and OT-R were detected on EC projections into the fetal lumen and OT-R on 20-150 nm clusters therein, prompting the hypothesis that placental exosomes transport OT-R to the fetus and across the blood-brain barrier. Insights on gestational complications were gained by univariable and multivariable regression analyses associating preeclampsia with lower MDMX protein levels in membrane extracts of chorionic villi, and lower MDMX, PICALM, OT-R, and V1aR with spontaneous vaginal deliveries compared to cesarean deliveries before the onset of labor. We found select associations between higher MDMX, PICALM, OT-R protein levels and either gravidity, diabetes, BMI, maternal age, or neonatal weight, and correlations only between PICALM-OT-R (p<2.7x10-8), PICALM-V1aR (p<0.006), and OT-R-V1aR (p<0.001). These results offer for exploration new partnerships in metabolic networks, tissue-resident immunity, and labor, notably for HC that predominantly express MDMX.
2024-05-22 | PXD050049 | Pride
Project description:OBJECTIVES: The Multi-Omics for Mothers and Infants (MOMI) consortium aims to improve birth outcomes. We analyzed full thickness placental samples (e.g., basal plate, placenta/chorionic villi and the chorionic plate) collected by the 5 MOMI sites: The Alliance for Maternal and Newborn Health Improvement (AMANHI) Bangladesh, AMANHI Pakistan, AMANHI Tanzania, The Global Alliance to Prevent Prematurity and Stillbirth (GAPPS) Bangladesh and GAPPS Zambia. STUDY DESIGN. The teams collected biopsies from 294 preterm (gestation <37 weeks) and 291 term (gestation ≥37 weeks) births. They were formalin-fixed and paraffin embedded. Tissue sections from these samples were stained with hematoxylin and eosin and subjected to morphological analyses. Other placental biopsies (n = 35 preterm, 21 term) were collected in RNAlater, which enabled bulk transcriptomics. RESULTS. The morphological analyses revealed a surprisingly high rate of inflammation involving the basal plate, placenta/chorionic villi and the chorionic plate. The rate in chorionic villus samples ranged from 25% (Pakistan site) to 60% (Zambia site) of cases. Leukocyte infiltration in this location vs. the basal plate or chorion plate correlated with preterm birth. The transcriptomic analyses identified 267 genes as differentially expressed (DE) between placentas from preterm vs. term births (123 upregulated, 144 downregulated). Mapping the DE genes onto single cell RNA-seq data from human placentas suggested that all the component cell types, either singly or in subsets, contributed to the observed dysregulation. Consistent with the histopathological findings, (Gene Ontology) GO analyses highlighted leukocyte infiltration/activation and inflammatory responses in both the fetal and maternal compartments. CONCLUSION. Together these data suggested geographic- and/or population-based differences in placental inflammation and the triggers of preterm birth.
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