Transcriptome profiling of control and FOSL1 knockdown Rcho-1 trophoblast stem (TS) cells
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
SUBMITTER: Kaiyu Kubota
PROVIDER: E-GEOD-68272 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:In hemochorial placentation, trophoblast stem cells differentiate into multiple lineages to aquire specific functions, such as invasive and endocrine phenotype. FOSL1 has been identified as a key regulator for trophoblast differentiation. We used microarray to detail mechanisms underlying FOSL1 signaling pathway in trophoblast differentiation.
2015-06-30 | GSE68272 | GEO
Project description:Trophoblast stem (TS) cell renewal and differentiation are essential processes in placentation. Here, we have identified the mechanism/targets of chromatin organizer/transcription factor called special AT-rich binding protein 1 (SATB1) action on TS cell renewal by RNA-seq analysis in Rcho-1 TS cells expressing Satb1 shRNAs.
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Project description:Placental abnormalities occur frequently in cloned animals. To investigate gene expression profile of trophoblast cell lineage of somatic cell nuclear transferred (NT) embryos, we established TS cells from blastocysts produced by NT at the blastocyst stage. Experiment Overall Design: Five independent TS cell lines derived from NT embryos were used in this study. Those included three lines from BDF1 background NT embryos and two lines from EGFP-Tg CD-1 background NT embryos. Two each of control lines, derived from native blastocysts of each background, were also used.
2009-08-07 | E-GEOD-17102 | biostudies-arrayexpress
Project description:Placental abnormalities occur frequently in cloned animals. To investigate DNA methylation profile of trophoblast cell lineage of somatic cell nuclear transferred (NT) embryos, we established TS cells from blastocysts produced by NT at the blastocyst stage. Three independent TS cell lines derived from NT embryos rom BDF1 background were used in this study. Two control lines, derived from native blastocysts of BDF1 background, were also used.
2010-05-16 | E-GEOD-17104 | biostudies-arrayexpress
Project description:During mammalian embryonic development, the first lineage commitment event gives rise to two distinct cell populations: the trophectoderm (TE) and the inner cell mass (ICM). The TE consists of outer cells of the blastocyst and ultimately forms the placenta while the ICM gives rise to all the embryonic tissues. Numerous transcription factors (TFs) guiding ICM differentiation into different embryonic tissues have been characterized. However, only a few TFs that are required for TE specification and differentiation have been identified, and much less is understood as to how these TFs interact with other TFs or with their chromosomal targets in order to drive cell fate towards TE lineage. Understanding trophectoderm development is crucial because cells in this lineage are required for proper embryo implantation in the uterus. Defects in this lineage can cause early failure of pregnancy as well as other pregnancy related disorders such as preeclampsia and intrauterine growth restriction (IUGR). Here, we characterize the function of one of TE-specific TF, Fosl1, which was previously suggested as having some role in placental development. We utilized mouse embryonic stem (ES) cells (derived from ICM) and showed that ectopic expression of Fosl1 can transdifferentiate ES cells to differentiated TS cells (trophoblast giant-like cells). We show that Fosl1 does so by directly binding and activating TE specific genes and genes associated with epithelial-mesenchymal transition (EMT). Using mouse trophoblast stem (TS) cells, we also establish that Fosl1 is required for specification of TS cells to trophoblast giant cells (TGCs) subtype. Therefore, we postulate that Fosl1 is a key regulator of TS cell differentiation.
2018-04-25 | GSE99983 | GEO
Project description:During mammalian embryonic development, the first lineage commitment event gives rise to two distinct cell populations: the trophectoderm (TE) and the inner cell mass (ICM). The TE consists of outer cells of the blastocyst and ultimately forms the placenta while the ICM gives rise to all the embryonic tissues. Numerous transcription factors (TFs) guiding ICM differentiation into different embryonic tissues have been characterized. However, only a few TFs that are required for TE specification and differentiation have been identified, and much less is understood as to how these TFs interact with other TFs or with their chromosomal targets in order to drive cell fate towards TE lineage. Understanding trophectoderm development is crucial because cells in this lineage are required for proper embryo implantation in the uterus. Defects in this lineage can cause early failure of pregnancy as well as other pregnancy related disorders such as preeclampsia and intrauterine growth restriction (IUGR). Here, we characterize the function of one of TE-specific TF, Fosl1, which was previously suggested as having some role in placental development. We utilized mouse embryonic stem (ES) cells (derived from ICM) and showed that ectopic expression of Fosl1 can transdifferentiate ES cells to differentiated TS cells (trophoblast giant-like cells). We show that Fosl1 does so by directly binding and activating TE specific genes and genes associated with epithelial-mesenchymal transition (EMT). Using mouse trophoblast stem (TS) cells, we also establish that Fosl1 is required for specification of TS cells to trophoblast giant cells (TGCs) subtype. Therefore, we postulate that Fosl1 is a key regulator of TS cell differentiation.
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Project description:Invasive trophoblast cells are critical to spiral artery remodeling in hemochorial placentation. Insufficient trophoblast invasion and vascular remodeling can lead to pregnancy disorders including preeclampsia, preterm birth, and intrauterine growth restriction. Previous studies in the mouse identified achaete-scute homolog 2 (ASCL2) as essential to extraembryonic development. We hypothesized that ASCL2 is a critical and conserved regulator of invasive trophoblast lineage development. In contrast to the mouse, the rat possesses deep intrauterine trophoblast cell invasion and spiral artery remodeling similar to human placentation. In this report, we investigated invasive/extravillous trophoblast (EVT) cell differentiation using human trophoblast stem (TS) cells and a loss-of-function mutant Ascl2 rat model. ASCL2 transcripts are expressed in the EVT column and junctional zone, which represent tissue sources of invasive trophoblast progenitor cells within human and rat placentation sites, respectively. Differentiation of human TS cells into EVT cells resulted in significant upregulation of ASCL2 and several other transcripts indicative of EVT cell differentiation. Disruption of ASCL2 impaired EVT cell differentiation as indicated by cell morphology and transcript profiles. RNA sequencing analysis of ASCL2-deficient trophoblast cells identified both downregulation of EVT cell-associated transcripts and upregulation of syncytiotrophoblast-associated transcripts, indicative of dual activating and repressing functions. ASCL2 deficiency in the rat impacted placental morphogenesis resulting in junctional zone dysgenesis and failed intrauterine trophoblast cell invasion. ASCL2 acts as a critical and conserved regulator of invasive trophoblast cell lineage development and a species-specific modulator of the syncytiotrophoblast lineage.
2021-03-01 | GSE154350 | GEO
Project description:The extravillous trophoblast (EVT) cell lineage is a key feature of placentation and critical for spiralartery remodeling and successful pregnancy. Our knowledge of transcriptional regulation driving EVT cell development is limited. Here, we mapped the transcriptome and epigenome landscape as well as chromatin interactions of human trophoblast stem (TS) cells and their transition into the differentiated EVT cell lineage. We identified that chromatin accessibility in intergenic regions was more extensive in EVT cells than in TS cells in the stem state, which is indicative of increased enhancer-driven gene regulation. Using reference epigenome annotation, we noted that 18% of the chromatin landscape in EVT cells was uncharted. We linked regulatory regions to their cognate target genes and characterized the three-dimensional organization of the TS cell functional genome by Hi-C. Integrational analysis of chromatin accessibility, long-range chromatin interactions, transcriptomic, and transcription factor binding motif enrichment enabled identification of transcription factors and regulatory mechanisms associated with EVT cell lineage development. Subsequent analyses elucidated functional roles forTFAP2C,EPAS1,SNAI1, andDLX6in the regulation of EVT cell lineage development.EPAS1was identified as an upstream regulator of EVT cell transcription factors, includingSNAI1andDLX6, and was found to be upregulated in idiopathic recurrent pregnancy loss. Collectively, we have revealed activation of a dynamic regulatory network that provides a framework for understanding EVT cell specification in trophoblast cell lineage development and human placentation.
2023-06-20 | GSE235271 | GEO
Project description:The extravillous trophoblast (EVT) cell lineage is a key feature of placentation and critical for spiralartery remodeling and successful pregnancy. Our knowledge of transcriptional regulation driving EVT cell development is limited. Here, we mapped the transcriptome and epigenome landscape as well as chromatin interactions of human trophoblast stem (TS) cells and their transition into the differentiated EVT cell lineage. We identified that chromatin accessibility in intergenic regions was more extensive in EVT cells than in TS cells in the stem state, which is indicative of increased enhancer-driven gene regulation. Using reference epigenome annotation, we noted that 18% of the chromatin landscape in EVT cells was uncharted. We linked regulatory regions to their cognate target genes and characterized the three-dimensional organization of the TS cell functional genome by Hi-C. Integrational analysis of chromatin accessibility, long-range chromatin interactions, transcriptomic, and transcription factor binding motif enrichment enabled identification of transcription factors and regulatory mechanisms associated with EVT cell lineage development. Subsequent analyses elucidated functional roles forTFAP2C,EPAS1,SNAI1, andDLX6in the regulation of EVT cell lineage development.EPAS1was identified as an upstream regulator of EVT cell transcription factors, includingSNAI1andDLX6, and was found to be upregulated in idiopathic recurrent pregnancy loss. Collectively, we have revealed activation of a dynamic regulatory network that provides a framework for understanding EVT cell specification in trophoblast cell lineage development and human placentation.
2023-06-20 | GSE235270 | GEO
Project description:The extravillous trophoblast (EVT) cell lineage is a key feature of placentation and critical for spiralartery remodeling and successful pregnancy. Our knowledge of transcriptional regulation driving EVT cell development is limited. Here, we mapped the transcriptome and epigenome landscape as well as chromatin interactions of human trophoblast stem (TS) cells and their transition into the differentiated EVT cell lineage. We identified that chromatin accessibility in intergenic regions was more extensive in EVT cells than in TS cells in the stem state, which is indicative of increased enhancer-driven gene regulation. Using reference epigenome annotation, we noted that 18% of the chromatin landscape in EVT cells was uncharted. We linked regulatory regions to their cognate target genes and characterized the three-dimensional organization of the TS cell functional genome by Hi-C. Integrational analysis of chromatin accessibility, long-range chromatin interactions, transcriptomic, and transcription factor binding motif enrichment enabled identification of transcription factors and regulatory mechanisms associated with EVT cell lineage development. Subsequent analyses elucidated functional roles forTFAP2C,EPAS1,SNAI1, andDLX6in the regulation of EVT cell lineage development.EPAS1was identified as an upstream regulator of EVT cell transcription factors, includingSNAI1andDLX6, and was found to be upregulated in idiopathic recurrent pregnancy loss. Collectively, we have revealed activation of a dynamic regulatory network that provides a framework for understanding EVT cell specification in trophoblast cell lineage development and human placentation.
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