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Severe damage on placental fetal capillary network causes mid to late fetal lethality and reduction of placental size in Peg11/Rtl1 KO mice [day 10.5]

ABSTRACT: Paternally expressed 11/Retrotransposon-like 1 (Peg11/Rtl1) knockout (KO) mice exhibited mid to late fetal lethality or late fetal growth retardation associated with frequent neonatal lethality. The lethal phenotype was largely dependent on genetic background and became more severe with each succeeding generation in the course of backcross experiments to C57BL/6 (B6). We previously suggested these lethal and growth phenotypes were due to severe defects in placental fetal capillaries in labyrinth layer. In this study, we reexamined KO fetuses exhibiting mid fetal lethality with internal bleeding. Importantly, basal region of fetal capillary network was specially damaged, therefore, also leading to poor expansion of the labyrinth layer and placental size reduction in later stage. Apparent up-regulation of Guanine nucleotide binding protein, alpha 2 (Gnai2) and decrement of Transmembrane protein 100 (Tmem100), Mesenchyme homeobox 2 (Meox2) and Lymphatic vessel hyaluronan Receptor 1 (LYVE1) expression were observed in earlier stage of placentas even before apparent morphological changes occurred, suggesting that these genes are involved in the maintenance of fetal capillaries associated with Peg11/Rtl1 in development.

ORGANISM(S): Mus musculus

PROVIDER: GSE88849 | GEO | 2016/10/19

SECONDARY ACCESSION(S): PRJNA349031

REPOSITORIES: GEO

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Severe damage on placental fetal capillary network causes mid to late fetal lethality and reduction of placental size in Peg11/Rtl1 KO mice [day 12.5]

Project description:Paternally expressed 11/Retrotransposon-like 1 (Peg11/Rtl1) knockout (KO) mice exhibited mid to late fetal lethality or late fetal growth retardation associated with frequent neonatal lethality. The lethal phenotype was largely dependent on genetic background and became more severe with each succeeding generation in the course of backcross experiments to C57BL/6 (B6). We previously suggested these lethal and growth phenotypes were due to severe defects in placental fetal capillaries in labyrinth layer. In this study, we reexamined KO fetuses exhibiting mid fetal lethality with internal bleeding. Importantly, basal region of fetal capillary network was specially damaged, therefore, also leading to poor expansion of the labyrinth layer and placental size reduction in later stage. Apparent up-regulation of Guanine nucleotide binding protein, alpha 2 (Gnai2) and decrement of Transmembrane protein 100 (Tmem100), Mesenchyme homeobox 2 (Meox2) and Lymphatic vessel hyaluronan Receptor 1 (LYVE1) expression were observed in earlier stage of placentas even before apparent morphological changes occurred, suggesting that these genes are involved in the maintenance of fetal capillaries associated with Peg11/Rtl1 in development.

2016-10-19 | GSE88891 | GEO

Severe damage on placental fetal capillary network causes mid to late fetal lethality and reduction of placental size in Peg11/Rtl1 KO mice

Project description:Severe damage on placental fetal capillary network causes mid to late fetal lethality and reduction of placental size in Peg11/Rtl1 KO mice

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Exposure to lipopolysaccharide induces sexually dimorphic placental adaptation by modifying placental efficiency, morphogenesis, and gene expression

Project description:Sexual dimorphism in placental physiology during development affects the functionality of placental adaptation during adverse pregnancy, affecting fetal growth, development, and eventually fetal programming, which have long-term effects on the offspring’s adult life. However, studies focusing on the phenomenon and relationship between sex-specific placental adaptation and consequent altered fetal development are still elusive. Here, we established a prenatal maternal stress model by administering lipopolysaccharide (LPS) to pregnant ICR mice at the mid-gestational stage. To verify the appropriateness of the animal model to study sex differences in the sub-optimal uterus milieu, pregnancy complications were examined. To elucidate global transcriptomic changes occurring in the placenta, total RNA sequencing was performed in female and male placentas. LPS exposure at the mid-gestational stage induced placental inflammation in both sexes. In utero inflammatory conditions resulted in intrauterine fetal growth restriction and impaired placental development in a sex-specific manner depending on the dose of LPS. Sex-biased placental pathology was observed in the junctional zone and the labyrinth layer. Placental transcriptome analysis revealed widespread disparity in protein-coding and long non-coding genes between female and male placentas, presenting the relationship between morphology and function in a sex-specific IUGR model.

2021-08-26 | GSE182462 | GEO

Maternal Influenza A Virus Infection Restricts Fetal and Placental Growth and Adversely Affects the Fetal Thymic Transcriptome

Project description:Maternal influenza A viral infections in humans are associated with low birth weight, increased risk of pre-term birth, stillbirth and congenital defects. To examine the effect of maternal influenza virus infection on placental and fetal growth, pregnant C57BL/6 mice were inoculated intranasally with influenza A virus A/CA/07/2009 pandemic H1N1 or PBS at E3.5, E7.5 or E12.5, and the placentae and fetuses collecgted and weighed at E18.5. Fetal thymuses were pooled from each litter. Placentae were examined histologically, stained by IHC for CD34 and vascular channels quantified. RNA from E7.5 and E12.5 placentae and E7.5 fetal thymuses was subjected to RNA sequencing and pathway analysis. Placental weights were decreased in litters inoculated with influenza at E3.5 and E7.5. Placentae from E7.5 and E12.5 inoculated litters exhibited decreased labyrinth development and transmembrane protein 150A gene was upregulated in E7.5 placentae. Fetal weights were decreased in litters inoculated at E7.5 and E12.5 compared to controls. RNA sequencing of E7.5 thymuses indicated that 957 genes were downregulated 2-fold including Mal, which is associated with Toll-like receptor signaling and T cell differentiation. There were 28 upregulated genes. It is concluded that maternal influenza A virus infection impairs fetal thymic gene expression as well as restricting placental and fetal growth.

2020-09-11 | GSE157132 | GEO

Expression of the placental transcriptome in fetal growth restriction in the Baboon is Dependent on Fetal Sex

Project description:Fetal growth restriction (FGR) develops when fetal nutrient availability is compromised and increases the risk for perinatal complications and predisposes for offspring obesity, diabetes and cardiovascular disease later in life. Emerging evidence implicates changes in placental function in altered fetal growth and the subsequent development of adult disease. The susceptibility for disease in response to an adverse intrauterine environment differs distinctly between boys and girls, with girls typically having better outcomes. Here, we test the hypothesis that regulation of the placental transcriptome by moderate nutrient reduction is dependent on fetal sex. We used a non-human primate model of FGR in which maternal global food intake is reduced by 30% starting at gestational day (GD) 30. At GD 165 (term = GD 183) placental genome expression profiling was carried out followed by bioinformatics including pathway and network analysis. Surprisingly, there was no coordinated placental molecular response to decreased nutrient availability when analyzing the data without accounting for fetal sex. In contrast, female placentas exhibited a highly coordinated response that included up-regulation of genes in networks, pathways and functional groups related to programmed cell death and down-regulation of genes in networks, pathways and functional groups associated with cell proliferation. These changes were not apparent in the male placentas. Our data support the concept that female placentas initiate complex adaptive responses to an adverse intrauterine environment, which may contribute to increased survival and better pregnancy outcomes in girls. Total RNA obtained from 165dGA control female (n=3), control male (n=3), nutrient restricted female (n=3), and nutrient restricted male (n=3) pregnancies.

2013-12-06 | E-GEOD-40878 | biostudies-arrayexpress

Expression of the placental transcriptome in fetal growth restriction in the Baboon is Dependent on Fetal Sex

2013-12-06 | GSE40878 | GEO

Mus musculus

Project description:Severe damage on placental fetal capillary network causes mid to late fetal lethality and reduction of placental size in Peg11/Rtl1 KO mice [day 10.5]

| PRJNA349031 | ENA

Mus musculus

Project description:Severe damage on placental fetal capillary network causes mid to late fetal lethality and reduction of placental size in Peg11/Rtl1 KO mice [day 12.5]

| PRJNA349030 | ENA

Alteration of LncRNA expression in mice placentae after frozen embryo transfer is associated with increased fetal weight.

Project description:Background: Frozen embryo transfer (FET) significantly upregulates fetal weight compared with fresh embryo transfer. However, the mechanism of FET increasing fetal weight remains unclear. Methods: We transferred blastocysts which had been vitrifified and warmed or fresh blastocysts into individual pseudopregnant recipients (n=11 mice each group) produced by natural mating to eliminate the influence of superovulation. The fetal weight, placental weight, placental efficiency and placenta architecture were compared. We performed placental lncRNA sequencing and mRNA sequencing to study the placental transcriptoms changes. And 15 selected differentially expressed lncRNAs and 15 mRNAs was checked. Findings: Enhanced birthweight (1.513 g vs. 1.685 g, P <0.001) was found in FET mice, with increased placental efficiency (11.355 vs. 10.312, P =0.045) and proportion of labyrinth zone area (59.78% vs. 53.19%, P = 0.034), indicating FET might change the placental function and morphology architecture. A total of placental 97608 mRNAs and 103339 lncRNAs were obtained, among which 1012 mRNAs and 554 lncRNAs showed significantly different expression between two groups. KEGG and GO enrichment analyses showed that the differentially expressed lncRNAs and their targeted mRNAs were related to labyrinth zone formation and maternal-fetal interface vascular remodeling. qRT-PCR, Western blotting and correlation analysis demonstrated that suppressed Lncenc1 to elevate Gjb5 might play a role in increased fetal weight of FET. Interpretation: FET changes the placental function and architecture resulting in higher mouse fetal weight, potentially via the network diagram of Lncenc1-miRNA-Gjb5.

2022-12-22 | GSE180310 | GEO

Mechanisms and function of de novo DNA methylation in placental development [PBAT]

Project description:DNA methylation is a repressive epigenetic modification that is essential for development, exemplified by the embryonic and perinatal lethality observed in mice lacking de novo DNA methyltransferases (DNMTs). Here we characterise the role for DNMT3A, 3B and 3L in gene regulation and development of the mouse placenta. We demonstrate that each of the DNMTs is required to establish the placental methylome and is distinctly targeted to genome based on underlying chromatin features. Loss of Dnmt3b results in de-repression of germline genes in trophoblast lineages and impaired development of the placental maternal-foetal interface. Critically, loss of DNA methylation in the placenta did not lead to abnormalities in lineage specification or cell identity, but to defective formation and vascularisation of the placental labyrinth. Using Sox2-Cre to delete Dnmt3b in the embryo, leaving expression intact in placental trophoblast cells, we were able to rescue the placental phenotype and, consequently, the embryonic lethality, as Dnmt3b null embryos could now survive to birth. We conclude that the principal function of DNA methylation during embryogenesis is to regulate placental function, which in turn is critical for embryo survival.

2022-12-15 | GSE203292 | GEO

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