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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE180310 | GEO | 2022/12/22

REPOSITORIES: GEO

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A long non-coding RNA specifically expressed in early embryos programs the metabolic balance in adult mice

Project description:Long non-coding RNAs (lncRNAs) display higher tissue-specificity than mRNAs. In particular, many lncRNAs are specifically expressed in early embryos, but the physiological functions of most of them remain largely unknown. Here, we show that deficiency of Lncenc1, a lncRNA specifically expressed in early embryos, results in an altered glucose and lipid balance in adult mice. Newly weaned lncenc1-deficient mice have been shown to display higher fasting blood glucose levels and to prefer to use lipids as a fuel source. When mice were fed a normal chow diet (NCD), in which glucose was the main energy source, glucose intolerance and insulin resistance were observed in adult lncenc1-deficient mice. Under high-fat diet (HFD) conditions, however, lncenc1-deficient mice became healthier and could resist food-induced obesity and metabolic disturbances, including liver steatosis and hypercholesterolmia. Furthermore, PPARγ-regulated lipogenesis in liver was reduced in lncenc1-deficient mice fed an HFD, as shown by transcriptome analyses. Interestingly, lncenc1-deficient mouse embryonic fibroblasts (MEFs) showed impaired glycolysis and lipogenesis, suggesting that the metabolic defects may already exist in embryos. Our study provides the first piece of evidence showing the essential roles of embryo-specific lncRNAs in adult metabolism, verifying the “fetal origin” of adult metabolic disorders.

2022-08-02 | GSE135314 | 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

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 [day 10.5]

2016-10-19 | GSE88849 | GEO

The Long Noncoding RNA Lncenc1 Regulates Glycolysis in Naive Mouse ES Cells II

Project description:The naive embryonic stem cells (nESCs) display unique characteristics mirroring naive pluripotency in vivo, but the molecular mechanisms underlying the self-renewal of nESCs remain incompletely understood. Here we analyzed stranded transcriptomes in mouse nESCs and epiblast-like cells (EpiLCs), and identified 135 long non-coding RNAs (lncRNAs) preferentially expressed in nESCs. We further investigated the functions of Lncenc1, a highly abundant lncRNA in mouse nESCs. Knockdown or knockout of Lncenc1 in mouse nESCs leads to significantly decreased expression of core pluripotency genes and significant reduction of colony formation capability. Furthermore, depletion of Lncenc1 down-regulates the glycolysis pathway, as indicated by significant decreases of glycolysis genes expression, glucose consumption, lactate production and Seahorse data. Mechanically, Lncenc1 associates with RNA-binding proteins PTBP1 and HNRNPK functionally. Together, we demonstrate that Lncenc1 regulates the glycolysis in mouse nESCs, suggesting novel functions of lncRNAs in linking energy metabolism and pluripotent stem cells.

2018-08-01 | GSE116462 | GEO

The Long Noncoding RNA Lncenc1 Regulates Glycolysis in Naive Mouse ES Cells I

2018-08-01 | GSE116458 | GEO

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

LncRNA and mRNA Sequencing Analysis of Left Testis in Experimental Varicocele Rats Treated with Morinda officinalis Polysaccharide

Project description:Purpose: Next-generation sequencing (NGS) was performed to illustrate the genetic molecular mechanism underlying varicocele (VC) pathogenesis and Morinda officinalis polysaccharide (MOP) repair effect. Methods: The male Sprague–Dawley (SD) rats (about 6-7 weeks old and 200±10g weight) were divided into three groups: 1) control group (Control); 2) experimental varicocele group (VC); 3) 300 mg kg-1 MOP administration group (VC+MOP). The next-generation RNA sequencing were performed to identify the differentially-expressed mRNA and lncRNA in left testicular tissue between each two compared group. Results: The result show that a total of 144 mRNAs and 63 LncRNAs, 63 mRNAs and 148 LncRNAs , 173 mRNAs and 54 LncRNAs were found differentially expressed between compared group VC vs. Control, VC+MOP vs. VC, and VC+MOP vs. Control respectively. Conclusions: Our study try to offer a indication for novel diagnose marker and therapeutic method, as well as provide feasible research orientations for further study.

2021-09-08 | GSE139447 | GEO

Effect of NDRG1 deletion and hypoxia in mouse placenta

Project description:We sought to identify changes in placental gene expression that may contribute to the phenotype of NDRG1-deficient embryos, and to define the contribution of hypoxia and fetal sex to these changes. We therefore used high-density oligonucleotide microarrays to interrogate differences in placental gene expression, stratified by fetal sex, Ndrg1 status (WT vs KO) and oxygenation (21% vs 12%).

2013-04-26 | GSE46381 | GEO

Transcription profiling of mouse placenta to determine the relative effects of maternal and fetal genotype on the placental transcriptome at E18.5

Project description:The placenta plays a crucial role in the normal growth and development in mammals by serving as an interface for nutrients, respiratory gases and physiological signals between the mother and fetus. Here we use a novel embryo transfer system in mice to identify the major physiological pathways in the placenta that are principally influenced by altered maternal environment. Embryos of identical genotype were transferred at the one cell stage into surrogate mothers either of the same strain or from a different strain. We analyzed the relative effects of maternal and fetal genotype on fetal weight, placental weight and the placental transcriptome at E18.5. The results show that maternal genotype overrides fetal genotype as the principal regulator of fetal weight (p<0.0001). Microarray analysis of the transcriptome in placentas revealed that a small fraction (0.25%) of placental genes are specifically regulated by maternal genotype (p<0.05, FDR<0.10). Pathway analysis of these genes using the programs Gene Ontology and MetaCore from GeneGO inc. revealed highest statistical significance in signaling pathways that regulate cell growth and lipid metabolism. These results provide a mechanistic understanding of important molecular pathways involved in maternal regulation of fetal growth and development.

2010-08-06 | E-MEXP-2479 | biostudies-arrayexpress

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