Modeling the Progression of Placental Transport from Early‐ to Late‐Stage Pregnancy by Tuning Trophoblast Differentiation and Vascularization
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE245763 | GEO | 2023/10/24
REPOSITORIES: GEO
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Project description:Modeling the Progression of Placental Transport from Early‐ to Late‐Stage Pregnancy by Tuning Trophoblast Differentiation and Vascularization
| PRJNA1029921 | ENA
Project description:Introduction: In human placenta, alteration in trophoblast differentiation has a major impact on placental maintenance and integrity. Moreover, abnormal syncytial fusion seems to be implicated in the development of many complications including pre-eclampsia and intra-uterine growth restriction (IUGR). However, little is known about the mechanisms that control cytotrophoblast fusion into syncytiotrophoblast. BeWo cell line is commonly used to study placental function since it can be induced to form syncytium and secretes hormones. This fusion is triggered by cAMP or forskolin treatments. In contrast, JEG-3 cell line fails to undergo substantial fusion. Therefore, we will use BeWo and JEG-3 cells to identify a set of genes responsible of trophoblast fusion. Methods: BeWo and JEG-3 cells were treated with forskolin for 48 to induce fusion. RNA was extracted, hybridized to Affymetrix HuGene ST1.0 arrays and analyzed using system biology. Trophoblast differentiation was evaluated by real time PCR and immunocytochemistry analysis. Moreover, some of the identified genes were validated by real time PCR. Results: Our results identified a list of 32 altered genes in fused BeWo cells compared to JEG-3 cells after forskolin treatment. Among these genes, 4 were validated by real-time PCR including salt inducible Kinase 1 (SIK1) gene which is specifically upregulated in BeWo cells upon fusion. Moreover, using system biology analysis, SIK1 showed to be at the center of many biological and functional processes which suggest that it might play a major role in trophoblast differentiation. Conclusion: This study identified new target genes implicated in trophoblast fusion; a process implicated in the etiology of many pregnancy-related diseases such as preeclampsia, IUGR, and gestational diabetes.
2019-02-26 | GSE127170 | GEO
Project description:Recent reports suggested human embryonic development is not always consistent with mouse. However, experimental approach to in vivo human embryos is extremely limited. Therefore, it is important to develop an appropriate in vitro cell culture system to analyse human pre-implantation development. In this report, we use human naive pluripotent stem cells (PSCs), which share features with pre-implantation epiblasts and show in vitro lineage specification of human trophoblast lineages. We successfully differentiated naive PSCs into trophectoderm, cytotrophoblast, syncytiotrophoblast, and extravillous trophoblast. Cytotrophoblasts could be cultured for long term as stem cells.
2021-04-07 | GSE144994 | GEO
Project description:Utero-placental growth and vascular development are critical for pregnancy establishment that may be altered by various factors including assisted reproductive technologies (ART), nutrition, or others, leading to compromised pregnancy. We hypothesized that placental vascularization and expression of angiogenic factors are altered early in pregnancies after transfer of embryos created using selected ART methods. Pregnancies were achieved through natural mating (NAT), or transfer of embryos from NAT (NAT-ET), or IVF or in vitro activation (IVA). Placental tissues were collected on day 22 of pregnancy. In maternal caruncles (CAR), vascular cell proliferation was less (P<0.05) for IVA than other groups. Compared with NAT, density of blood vessels was less (P<0.05) for IVF and IVA in fetal membranes (FM) and for NAT-ET, IVF, and IVA in CAR. In FM, mRNA expression was decreased (P<0.01-0.08) in NAT-ET, IVF, and IVA compared with NAT for vascular endothelial growth factor (VEGF) and its receptor FLT1, placental growth factor (PGF), neuropilin 1 (NP1) and NP2, angiopoietin 1 (ANGPT1) and ANGPT2, endothelial nitric oxide synthase 3 (NOS3), hypoxia-inducible factor 1A (HIF1A), fibroblast growth factor 2 (FGF2), and its receptor FGFR2. In CAR, mRNA expression was decreased (P<0.01-0.05) in NAT-ET, IVF, and IVA compared with NAT for VEGF, FLT1, PGF, ANGPT1, and TEK. Decreased mRNA expression for 12 of 14 angiogenic factors across FM and CAR in NAT-ET, IVF, and IVA pregnancies was associated with reduced placental vascular development, which would lead to poor placental function and compromised fetal and placental growth and development.
| S-EPMC3981880 | biostudies-literature
Project description:BeWo trophoblast cells differentiate in response to expsure to cyclic adenosine monophosphate (cAMP) analogs. Differentiation includes syncytialization (fusion) and hormonogenesis. The goal of this study was to globally determine transcripts differentially expressed in BeWo trophoblast cells following a 24-h exposure to 250 uM 8-bromo-cAMP. 3 replicates undifferentiated BeWo trophoblast cells; and 3 replicates BeWo trophoblast cells treated with 250 uM 8-Br-cAMP for 24 h.
2015-08-01 | E-GEOD-66840 | biostudies-arrayexpress
Project description:Iron deficiency, which occurs when iron demands chronically exceed intake, is prevalent in pregnant women. Iron deficiency during pregnancy poses major risks for the baby, including fetal growth restriction and long-term health complications. The placenta serves as the interface between a pregnant mother and her baby, and it ensures adequate nutrient provisions for the fetus. Thus, maternal iron deficiency may impact fetal growth and development by altering placental function. We used a rat model of diet-induced iron deficiency to investigate changes in placental growth and development. Pregnant Sprague-Dawley rats were fed either a low-iron or iron-replete diet starting 2 weeks before mating. Compared with controls, both maternal and fetal hemoglobin were reduced in dams fed low-iron diets. Iron deficiency decreased fetal liver and body weight, but not brain, heart, or kidney weight. Placental weight was increased in iron deficiency, due primarily to expansion of the placental junctional zone. The stimulatory effect of iron deficiency on junctional zone development was recapitulated in vitro, as exposure of rat trophoblast stem cells to the iron chelator deferoxamine increased differentiation toward junctional zone trophoblast subtypes. Gene expression analysis revealed 464 transcripts changed at least 1.5-fold (P < 0.05) in placentas from iron-deficient dams, including altered expression of genes associated with oxygen transport and lipoprotein metabolism. Expression of genes associated with iron homeostasis was unchanged despite differences in levels of their encoded proteins. Our findings reveal robust changes in placentation during maternal iron deficiency, which could contribute to the increased risk of fetal distress in these pregnancies.
| S-EPMC8559528 | biostudies-literature
Project description:Comparison of genes associated with the EMT between trophoblast cell line (BeWo, JEG3) controls and cells overexpressing the ZEB2 gene (BeWo ZEB2oe, JEG_ZEB2oe).
2018-10-01 | GSE116532 | GEO
Project description:We report the transcriptomes of human choriocarcinoma cell lines JEG3 and BeWo in order to provide information about genes expressed by human trophoblasts.
2019-05-25 | GSE131753 | GEO
Project description:It has been confirmed that improving the energy level of the diet contributed to the greater reproductive performance and birth weight of calves in periparturient dairy cows. To investigate the effect of glucose on nutrient transport during fetal development, the bovine placental trophoblast cells (BPTCs) were cultured in media with different glucose concentrations (1, 2, 4, 8, or 16 mg/mL). Subsequently, the BPTCs were cultured in media with 1, 8 mg/mL glucose and 8 mg/mL glucose plus 100 nmol/L rapamycin (the inhibitor of mTOR pathway). Compared with the 1 mg/mL glucose, the addition of 8 mg/mL glucose stimulated cell proliferation, upregulated the mRNA abundance of the glucose transporter GLUT1 and GLUT4, and increased the activity of glucose metabolism-related enzyme glucose-6-phosphate dehydrogenease (G6PD), lactate dehydrogenase (LDHA) and phosphoglycerate kinase 1 (PGK1), as well as adenosine-triphosphate (ATP) content (p < 0.05).Furthermore, compared with the treatment of 1 mg/mL glucose, adding 8 mg/mL of glucose-upregulated gene expression in the mTOR signaling pathway, including phosphatidylinositol3-kinase (PI3K), protein kinase B (Akt), mammalian target of rapamycin (mTOR) and 70 kDa ribosomal protein S6 kinase 2 (P70S6K) (p < 0.05).The supplementation of rapamycin downregulated the gene and protein expression of the mTOR signaling pathway, including mTOR, P70S6K, EIF4E-binding protein 1 (4EBP1), hypoxia-inducible factor 1-alpha (HIF-1α) and gene expression of glucose transporter upregulated by 8 mg/mL glucose (p < 0.05). Thus, these results indicated that the addition of 8 mg/mL glucose regulated the glucose transport and metabolism in BPTCs through the mTOR signaling pathway, thereby promoting the supply of nutrients to fetus.
| S-EPMC10778405 | biostudies-literature
Project description:BeWo trophoblast cells differentiate in response to expsure to cyclic adenosine monophosphate (cAMP) analogs. Differentiation includes syncytialization (fusion) and hormonogenesis. The goal of this study was to globally determine transcripts differentially expressed in BeWo trophoblast cells following a 24-h exposure to 250 uM 8-bromo-cAMP.
2015-08-01 | GSE66840 | GEO