Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA151733 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Antiphospholipid antibodies, a maternal risk factor for preeclampsia, increase shedding of necrotic trophoblast debris from the placenta, leading to endothelial dysfunction. Using Affymetrix HGU133 Plus 2 microarrays, we found changes in the transcriptome of placental explants treated with antiphospholipid antibodies including seven mRNAs encoding for genes BCL2L1, MCL1, PDCD2L, FASLG, SEMA6A, PRKCE and TRAIL that are involved in the regulation of apoptosis. Quantitative real-time RT-PCR and immunohistochemistry confirmed a reduction in TRAIL expression. These results may help to understand how antiphospholipid antibodies affect trophoblast cell death and how the antibodies could contribute to the pathogenesis of preeclampsia.
2012-02-27 | GSE36083 | GEO
Project description:Antiphospholipid antibodies, a maternal risk factor for preeclampsia, increase shedding of necrotic trophoblast debris from the placenta, leading to endothelial dysfunction. Using Affymetrix HGU133 Plus 2 microarrays, we found changes in the transcriptome of placental explants treated with antiphospholipid antibodies including seven mRNAs encoding for genes BCL2L1, MCL1, PDCD2L, FASLG, SEMA6A, PRKCE and TRAIL that are involved in the regulation of apoptosis. Quantitative real-time RT-PCR and immunohistochemistry confirmed a reduction in TRAIL expression. These results may help to understand how antiphospholipid antibodies affect trophoblast cell death and how the antibodies could contribute to the pathogenesis of preeclampsia. Three different first-trimester placentas (8-8.5 weeks gestation) were dissected into 6 explants each and cultured either with antiphospholipid antibodies (25ug/mL) or untreated media for 16h. RNA was extracted from treated placental explants and Affymetrix HGU133 Plus 2 arrays were conducted to investigate changes in mRNA expression. Untreated: 1UNT, 2UNT, 3UNT Antiphospholipid antibody treatment: 1APL, 2APL, 3APL Biological replicates: 1, 2, 3
2012-02-27 | E-GEOD-36083 | biostudies-arrayexpress
Project description:The aim of this microarray experiment was to compare the overall transcriptomic profile of human placenta derived trophoblast organoid cultures with its tissue of origin, human placental villi. As the placental villi contains both trophoblast and stromal populations, we have included placenta derived stromal cultures in this comparison.
2018-11-28 | E-MTAB-6683 | biostudies-arrayexpress
Project description:Transcriptomic analysis confirms the trophoblast identity of the naïve pluripotent stem cell derived TSC cultures by comparing to the placenta derived TSC culture.
2021-02-20 | GSE167089 | GEO
Project description:Antiphospholipid syndrome (APS) is an autoimmune thrombophillia characterized by recurrent thrombotic events and/or pregnancy morbidity in the presence of antiphospholipid antibodies detected either as anti-cardiolipin, anti-β2 Glycoprotein I (anti-β2GPI) or Lupus anticoagulant (LA). Endothelial deregulation characterizes the syndrome. To address the gene expression changes occurring in the endothelial cells in the context of APS, we performed transcriptome analysis of Human Umbilical Vein Endothelial cells (HUVECs) stimulated with anti-β2GPI-β2GPI complexes.
2023-05-24 | GSE143506 | GEO
Project description:Trophoblast lineages, as the precursor of placenta, are essential for post-implantation embryo survival. However, the regulatory networks for trophoblast development remains incompletely understood. Here, we identified CITED1 as a regulator to induce trophoblast-like differentiation from mESCs. Overexpression of CITED1 in ESCs prompted differentiation towards trophoblast accompanying with elevated expression of trophoblast marker genes. To evaluate the ability of CITED1 to induce trophoblast differentiation at a genome-wide scale, we compared the global transcriptional profiles between CITED1 overexpressing cells and control ESCs by Affymetrix microarray analysis at day 1 and day 2 after transfection. We used microarrays to identify genes affected by CITED1 overexpression in mouse ESCs.
2018-09-01 | GSE103414 | GEO
Project description:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a well-known inducer of apoptosis via formation of the primary death-inducing signaling complex (TRAIL-DISC) at the level of membrane death receptors (DR4 and DR5) which recruit successively FADD and caspase-8. TRAIL can also induce necroptosis when caspases are inhibited. Necroptosis is a regulated cell death dependent on the formation of a cytosolic necrosome complex which includes RIPK1, RIPK3 and MLKL proteins. Elucidating the molecular mechanisms involved in TRAIL-induced necroptosis might provide new insights into the TRAIL death signaling pathway. Here, we report the analysis by mass spectrometry of endogenous RIPK3-dependent necrosome complex constituents upon necroptosis induced by TRAIL/z-VAD/Birinapant (TzB) in HT29 cells. Besides characterization of RIPK1, RIPK3, MLKL, FADD, caspase-8, we find TRIM21 as a new constituent of the necrosome complex. Moreover RIPK1, RIPK3, MLKL, P-MLKL, FADD, caspase-8 and TRIM21 are also found associated to the native TRAIL-DISC upon TzB stimulation showing initiation of the necrotic pathway at the level of TRAIL death receptors in HT29 cells. Finally, TRIM21 may positively modulate necroptosis induction by downregulating NF-kB activation.
2021-03-18 | PXD003383 | Pride
Project description:We established an immortalized term placenta-derived trophoblast cell line and demonstrated functional and transcriptomic differences against chorion trophoblasts and BeWo cells.
2024-10-23 | GSE250585 | GEO
Project description:The placenta is a poorly understood yet vital support organ. Transcriptome analysis at single cell resolution can help us understand cell compositions, developmental processes, and physiological functions. Both mice and humans have the hemochorial placenta. Profiling the single cell transcriptome of the mouse placenta is necessary for deepening our knowledge of mammalian placentation.We systematically profiled single cell transcriptomes of mouse placentae every day from E7.5 to E14.5. After stringent filtering, 15682 mouse trophoblast cells were subjected to following transcriptome analysis. We noted that trophoblast cells underwent 3 main differentiation stages: E7.5-E8.5, E9.5-E10.5, and E11.5-E14.5. With the help of advanced computational technologies from Velocyto, PAGA, monocle, and SCENIC, we have updated the recognitions of several developmental events. Firstly, P-TGCs are suggested to only derive from EPC like cells. Secondary, sinusoid trophoblast and spongiotrophoblast all derived from EPC cells, and their cell fates have been determined before the chorioallantoic fusion. Sinusoid trophoblast cells were not derived from chorion. Thirdly, SpA-TGCs were suggested to be differentiated from spongiotrophoblast cells via Gly-T cells. Furthermore, new transcription factors have been found to play roles during the differentiation of trophoblast cells. Lastly, the expression of Ifnlr1 in chorion branch cells gradually increased during placentation, which reconfirmed that mature placenta can defend the Zika virus (ZIKV) through IFN signaling. We clarified the developmental histories of mouse trophoblast cells at the branch level, especially the differentiation of sinusoid branch trophoblast cells. Meanwhile, we offered a convincing data resource for the study of mammalian placentation and etiology analysis of pregnancy-associated diseases.
2023-01-10 | GSE156125 | GEO
Project description:Clinical applications of human interferon (IFN)-alpha have met with varying degrees of success. Nevertheless, key molecules in IFN-alpha-induced cell death have not been clearly identified. Our previous study indicated that IFN (alpha, beta and omega) receptor (IFNAR) 1/2- and IFN regulatory factor (IRF) 9-RNA interference (RNAi) completely inhibited the antiproliferative (AP) activity of IFN-alpha in human ovarian adenocarcinoma OVCAR3 cells sensitive to IFN-alpha., followed by transcription of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Here, IFNAR1/2- and IRF9-RNAi inhibited the gene expression of TRAIL, but not of Fas ligand (FasL), following IFN-alpha treatment. In fact, TRAIL but not FasL inhibited the proliferation of OVCAR3 cells. IFN-alpha notably up-regulated the levels of TRAIL protein in the supernatant and on the membrane of OVCAR3 cells. Following TRAIL signaling, Caspase 8 inhibitor and BH3 interacting domain death agonist (BID)-RNAi significantly abrogated both AP activities of IFN-alpha and TRAIL. Furthermore, BID-RNAi prevented both IFN-alpha and TRAIL from collapsing the mitochondrial membrane potential (Delta Psi m). Finally, we provide important new evidence that BID overexpression led to a major enhancement of both AP activities of IFN-alpha and TRAIL in human lung carcinoma A549 cells resistant to IFN-alpha. Thus, this study suggests that BID is crucial in IFN-alpha-induced cell death, indicating a notable potential to be a targeted therapy for IFN-alpha resistant tumors.
2012-05-22 | GSE29790 | GEO