Transcriptome profiling of control and FOSL1 knockdown Rcho-1 trophoblast stem (TS) cells
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE68272 | GEO | 2015/06/30
SECONDARY ACCESSION(S): PRJNA282343
REPOSITORIES: GEO
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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. 3 replicates of differentiated Rcho1 TS cells expressing control shRNA; 3 replicates of differentiated Rcho1 TS cells expressing Fosl1 shRNA
2015-06-30 | E-GEOD-68272 | 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 | GSE99984 | 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.
2018-04-25 | GSE99983 | GEO
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.
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Project description:Placenta enriched 1 (PLAC1) is a highly conserved X chromosome-linked gene prominently expressed in the mammalian placenta. The functions of PLAC1 in placentation have yet to emerge fully. The rat shares hemochorial placentation and deep intrauterine trophoblast cell invasion with the human. Herein, we investigated the expression and biological activities of PLAC1 in the rat and human placenta. Plac1 transcripts were prominently expressed in the junctional zone of the rat placenta, a structure analogous to the extravillous trophoblast cell column of the human placentation site, and in invasive trophoblast cells. A PLAC1 mutant rat model was generated using CRISPR/Cas9 genome editing and used to investigate the role of PLAC1 in rat placentation. Plac1 mutant animals exhibited placentomegaly. Enlarged placentas were characterized by an expanded junctional zone, an irregular junctional zone-labyrinth zone boundary, and a prominent depletion of invasive trophoblast cells within the uterine parenchyma. PLAC1 was required for rat trophoblast stem (TS) cell differentiation. In human TS cell development, PLAC1 does not contribute to the regulation of the human invasive/extravillous trophoblast cell lineage, but instead, PLAC1 expression and actions were linked to syncytiotrophoblast differentiation. Thus, PLAC1 is critically involved in hemochorial placentation; however, the responsive trophoblast cell lineages and its contributions to placentation are fundamentally distinct in the rat versus human.
2026-04-22 | GSE263207 | GEO
Project description:Placenta enriched 1 (PLAC1) is a highly conserved X chromosome-linked gene prominently expressed in the mammalian placenta. The functions of PLAC1 in placentation have yet to emerge fully. The rat shares hemochorial placentation and deep intrauterine trophoblast cell invasion with the human. Herein, we investigated the expression and biological activities of PLAC1 in the rat and human placenta. Plac1 transcripts were prominently expressed in the junctional zone of the rat placenta, a structure analogous to the extravillous trophoblast cell column of the human placentation site, and in invasive trophoblast cells. A PLAC1 mutant rat model was generated using CRISPR/Cas9 genome editing and used to investigate the role of PLAC1 in rat placentation. Plac1 mutant animals exhibited placentomegaly. Enlarged placentas were characterized by an expanded junctional zone, an irregular junctional zone-labyrinth zone boundary, and a prominent depletion of invasive trophoblast cells within the uterine parenchyma. PLAC1 was required for rat trophoblast stem (TS) cell differentiation. In human TS cell development, PLAC1 does not contribute to the regulation of the human invasive/extravillous trophoblast cell lineage, but instead, PLAC1 expression and actions were linked to syncytiotrophoblast differentiation. Thus, PLAC1 is critically involved in hemochorial placentation; however, the responsive trophoblast cell lineages and its contributions to placentation are fundamentally distinct in the rat versus human.
2026-04-22 | GSE263209 | GEO
Project description:Placenta enriched 1 (PLAC1) is a highly conserved X chromosome-linked gene prominently expressed in the mammalian placenta. The functions of PLAC1 in placentation have yet to emerge fully. The rat shares hemochorial placentation and deep intrauterine trophoblast cell invasion with the human. Herein, we investigated the expression and biological activities of PLAC1 in the rat and human placenta. Plac1 transcripts were prominently expressed in the junctional zone of the rat placenta, a structure analogous to the extravillous trophoblast cell column of the human placentation site, and in invasive trophoblast cells. A PLAC1 mutant rat model was generated using CRISPR/Cas9 genome editing and used to investigate the role of PLAC1 in rat placentation. Plac1 mutant animals exhibited placentomegaly. Enlarged placentas were characterized by an expanded junctional zone, an irregular junctional zone-labyrinth zone boundary, and a prominent depletion of invasive trophoblast cells within the uterine parenchyma. PLAC1 was required for rat trophoblast stem (TS) cell differentiation. In human TS cell development, PLAC1 does not contribute to the regulation of the human invasive/extravillous trophoblast cell lineage, but instead, PLAC1 expression and actions were linked to syncytiotrophoblast differentiation. Thus, PLAC1 is critically involved in hemochorial placentation; however, the responsive trophoblast cell lineages and its contributions to placentation are fundamentally distinct in the rat versus human.
2026-04-22 | GSE263205 | GEO
Project description:Placenta enriched 1 (PLAC1) is a highly conserved X chromosome-linked gene prominently expressed in the mammalian placenta. The functions of PLAC1 in placentation have yet to emerge fully. The rat shares hemochorial placentation and deep intrauterine trophoblast cell invasion with the human. Herein, we investigated the expression and biological activities of PLAC1 in the rat and human placenta. Plac1 transcripts were prominently expressed in the junctional zone of the rat placenta, a structure analogous to the extravillous trophoblast cell column of the human placentation site, and in invasive trophoblast cells. A PLAC1 mutant rat model was generated using CRISPR/Cas9 genome editing and used to investigate the role of PLAC1 in rat placentation. Plac1 mutant animals exhibited placentomegaly. Enlarged placentas were characterized by an expanded junctional zone, an irregular junctional zone-labyrinth zone boundary, and a prominent depletion of invasive trophoblast cells within the uterine parenchyma. PLAC1 was required for rat trophoblast stem (TS) cell differentiation. In human TS cell development, PLAC1 does not contribute to the regulation of the human invasive/extravillous trophoblast cell lineage, but instead, PLAC1 expression and actions were linked to syncytiotrophoblast differentiation. Thus, PLAC1 is critically involved in hemochorial placentation; however, the responsive trophoblast cell lineages and its contributions to placentation are fundamentally distinct in the rat versus human.
2026-04-22 | GSE263213 | GEO
Project description:Placenta enriched 1 (PLAC1) is a highly conserved X chromosome-linked gene prominently expressed in the mammalian placenta. The functions of PLAC1 in placentation have yet to emerge fully. The rat shares hemochorial placentation and deep intrauterine trophoblast cell invasion with the human. Herein, we investigated the expression and biological activities of PLAC1 in the rat and human placenta. Plac1 transcripts were prominently expressed in the junctional zone of the rat placenta, a structure analogous to the extravillous trophoblast cell column of the human placentation site, and in invasive trophoblast cells. A PLAC1 mutant rat model was generated using CRISPR/Cas9 genome editing and used to investigate the role of PLAC1 in rat placentation. Plac1 mutant animals exhibited placentomegaly. Enlarged placentas were characterized by an expanded junctional zone, an irregular junctional zone-labyrinth zone boundary, and a prominent depletion of invasive trophoblast cells within the uterine parenchyma. PLAC1 was required for rat trophoblast stem (TS) cell differentiation. In human TS cell development, PLAC1 does not contribute to the regulation of the human invasive/extravillous trophoblast cell lineage, but instead, PLAC1 expression and actions were linked to syncytiotrophoblast differentiation. Thus, PLAC1 is critically involved in hemochorial placentation; however, the responsive trophoblast cell lineages and its contributions to placentation are fundamentally distinct in the rat versus human.
2026-04-22 | GSE263212 | GEO
Project description:Placenta enriched 1 (PLAC1) is a highly conserved X chromosome-linked gene prominently expressed in the mammalian placenta. The functions of PLAC1 in placentation have yet to emerge fully. The rat shares hemochorial placentation and deep intrauterine trophoblast cell invasion with the human. Herein, we investigated the expression and biological activities of PLAC1 in the rat and human placenta. Plac1 transcripts were prominently expressed in the junctional zone of the rat placenta, a structure analogous to the extravillous trophoblast cell column of the human placentation site, and in invasive trophoblast cells. A PLAC1 mutant rat model was generated using CRISPR/Cas9 genome editing and used to investigate the role of PLAC1 in rat placentation. Plac1 mutant animals exhibited placentomegaly. Enlarged placentas were characterized by an expanded junctional zone, an irregular junctional zone-labyrinth zone boundary, and a prominent depletion of invasive trophoblast cells within the uterine parenchyma. PLAC1 was required for rat trophoblast stem (TS) cell differentiation. In human TS cell development, PLAC1 does not contribute to the regulation of the human invasive/extravillous trophoblast cell lineage, but instead, PLAC1 expression and actions were linked to syncytiotrophoblast differentiation. Thus, PLAC1 is critically involved in hemochorial placentation; however, the responsive trophoblast cell lineages and its contributions to placentation are fundamentally distinct in the rat versus human.
2026-04-22 | GSE263211 | GEO