Effect of ferroportin on placental gene expression
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE206109 | GEO | 2022/11/18
REPOSITORIES: GEO
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Project description:Background: Maternal iron deficiency (ID) is associated with poor pregnancy and fetal outcomes. The effect is thought to be mediated by the placenta but there is no comprehensive assessment of placental response to maternal ID. Additionally, whether the influence of maternal ID on the placenta differs by fetal sex is unknown. Objectives: Our primary aim was to identify gene and protein signatures of ID mouse placentas at mid-gestation. A secondary objective was to profile the expression of iron genes in mouse placentas across gestation. Methods: We used a real-time PCR based array to determine the mRNA expression of all known iron genes in mouse placentas at embryonic day (E) 12.5, E14.5, E16.5, and E19.5 (n=3 placentas/time point). To determine the effect of maternal ID, we performed RNA sequencing and proteomics in male and female placentas from ID and iron adequate mice at E12.5 (n=8 dams/diet). Results: In female placentas, six genes including transferrin receptor (Tfrc) and solute carrier family 11 member 2 were significantly changed by maternal ID. An additional 154 genes were altered in male ID placentas. Proteomic analysis quantified 7662 proteins in the placenta. Proteins translated from iron responsive element (IRE) containing mRNAs were altered in abundance; ferritin and ferroportin 1 decreased while TFRC increased in ID placenta. Less than 4% of the significantly altered genes in ID placentas occurred both at the transcriptional and translational levels. Conclusions: Our data demonstrate that the impact of maternal ID on placental gene expression in mice is limited in scope and magnitude at mid-gestation. We provide strong evidence for IRE-based transcriptional and translational coordination of iron gene expression in the mouse placenta. Finally, we discover sexually dimorphic effects of maternal ID on placental gene expression, with more genes and pathways altered in male compared with female mouse placentas.
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Project description:As susceptibility to many adult disorders originates in utero, we here hypothesized that fetal sex influences gene expression in placental cells and produces functional differences in human placentas. We found that fetal sex differentially affects gene expression in a cell-phenotype dependent manner among all four placental cell-phenotypes studied: cytotrophoblasts, syncytiotrophoblasts, arterial endothelial cells and venous endothelial cells. The markedly enriched pathways in males were identified to be signaling pathways for graft-versus-host disease as well as the immune and inflammatory systems, both supporting the hypothesis that there is reduced maternal-fetal compatibility for male fetuses. Our study is the first microarray study investigating sexual dimorphism in purified and characterized somatic cells from a single human tissue, the placenta, that underlines the importance of considering fetal sex as an independent variable in any work using human placenta. Arterial and venous endothelial cells were isolated from eight different placentas, four of each sex. A total of ten placentas were used for isolation of cytotrophoblasts and six for syncytiotrophoblasts, with equal numbers from each sex.
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Project description:Effect of ferroportin on placental gene expression
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Project description:To understand the underlying cause and mechanisms of embryonic lethality observed in combined loss of E2f7 and E2f8, we compared global gene expression profiles of wild type, germline deleted and sox2-Cre/Cyp19-Cre deleted embryos and placentas. RNA was extracted from E10.5 embryos and placentas. Gene deletion in samples confirmed by PCR genotyping of DNA isolated from each sample.
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Project description:The mouse placenta forms primarily from cells in the trophectoderm (TE) of the blastocyst. Complicated lineage specification in placental trophoblast cells finally forms the functional placenta. However, at which stage the fate of mouse trophoblast lineages is determined key open questions. Lineage tracing is the most reliable approach to study cell fate determination. Herein, we took advantage of a fluorescent Cre recombinase reporter mouse for our lineage tracing experiments. Cell labeling experiments were performed by microinjection of Cre mRNA into single blastomere respectively at the two-, four- and eight-cell stage, and increasing bias of the labeled cell distribution was observed in the E12.5 fetus and placenta, which was also supported by the single cell sequencing results.Together, our data provide direct evidence supporting the idea that the first cell fate choice of early blastomeres, toward the inner cell mass (ICM) or trophoblast fate, has become determined at the four-cell stage, and three different cell fates may exist among the four blastomeres.Compared with previous studies, it is the first study to trace the cell lineages from early stages over such a long developmental period.
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