Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA323469 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3590620_1.fastq.gz | Fastqsanger.gz | |||
| SRR3590620_2.fastq.gz | Fastqsanger.gz | |||
| SRR3590615_1.fastq.gz | Fastqsanger.gz | |||
| SRR3590615_2.fastq.gz | Fastqsanger.gz | |||
| SRR3590616_1.fastq.gz | Fastqsanger.gz |
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Project description:Epithelial membrane protein-2 (EMP2) is a tetraspan protein predicted to regulateplacental development. Highly expressed in secretory endometrium and trophectoderm cells, previous studies suggest that it may regulate implantation by orchestrating the surface expression of integrins and other membrane proteins. In order to confirm the role of EMP2 in pregnancy, mice lacking EMP2 (Emp2-/- ) were generated. These animals are fertile but have reduced litter sizes. Moreover, their placentas exhibit dysregulation in pathways related to neoangiogenesis, coagulation, and oxidative stress, and have increased fibrin deposition and altered vasculature. Given that these findings often occur due to placental insufficiency resulting in an oxygen-poor environment, expression of hypoxia-inducible factor-1 alpha (HIF-1α) was examined. Emp2-/- animals have reduced HIF-1α expression within cells of trophoblast origin. However, they appear to have a compensatory increase in uterine NK (uNK) cells, demonstrating a unique interplay between uNK cells and trophoblasts modulated through EMP2. To determine if these results translated to human pregnancy, placentas from normal, term deliveries or those complicated by intrauterine growth restriction (IUGR) were stained for EMP2. EMP2 was significantly reduced in both villous and extravillous trophoblast populations in IUGR placentas. Experiments in vitro using human trophoblast cells lines indicate that EMP2 modulates angiogenesis by altering HIF-1a expression. Our results reveal a novel role for EMP2 in regulating trophoblast function and vascular development in conditions of altered oxygen availability in mice and humans and suggest it may be a novel biomarker for placental insufficiency.
2017-02-23 | GSE81940 | GEO
Project description:Placental insufficiency leading to intrauterine growth restriction demonstrates perturbed gene expression affecting placental angiogenesis and nutrient transfer from mother to fetus. To understand the post-transcriptional mechanisms underlying such placental gene expression changes, our objective was to identify key non-coding microRNAs that express biological function. To this end, we undertook microarray targeting microRNAs in placentas of appropriate (AGA, n=3) versus small for gestational age (SGA, n=3) weight infants and observed upregulation of 97 miRs in SGA versus AGA. In a larger cohort of samples, we validated by qRT-PCR, differential expression of three specific microRNAs that target genes mediating angiogenesis and nutrient transfer. We performed microarray on a small cohort of samples in order to identify differential expression in pathways involved with angiogenesis and nutrient transfer, essential processes for placental function that when perturbed, may result in intrauterine growth restriction.
2017-01-06 | GSE93174 | GEO
Project description:Placental insufficiency leading to intrauterine growth restriction demonstrates perturbed gene expression affecting placental angiogenesis and nutrient transfer from mother to fetus. To understand the post-transcriptional mechanisms underlying such placental gene expression changes, our objective was to identify key non-coding microRNAs that express biological function. To this end, we undertook microarray targeting microRNAs in placentas of appropriate (AGA, n=3) versus small for gestational age (SGA, n=3) weight infants and observed upregulation of 97 miRs in SGA versus AGA. In a larger cohort of samples, we validated by qRT-PCR, differential expression of three specific microRNAs that target genes mediating angiogenesis and nutrient transfer. This dataset was used to verify initial studies. We performed a second microarray on a small cohort of samples in order to validate differential expression in pathways involved with angiogenesis and nutrient transfer, essential processes for placental function that when perturbed, may result in intrauterine growth restriction.
2017-04-01 | GSE97294 | GEO
Project description:Pathologic retinal neovascularization is a potentially blinding consequence seen in many common diseases including diabetic retinopathy, retinopathy of prematurity, and retinal vascular occlusive diseases, among others. The use of therapeutics targeting pro-angiogenesis factors such as vascular endothelial growth factor (VEGF) has proven to be highly effective, however considerable side effects exist and serial anti-VEGF treatment has been shown to decrease effectiveness over time. Characterization of additional regulators of neovascularization is needed to further understand neovascular disease and identify possible new therapeutic targets. This study investigates epithelial membrane protein 2 (EMP2) and its role as a possible modulator of angiogenesis in human retinal pigment epithelium (RPE) under hypoxia. EMP2 is highly expressed in human RPE and RPE cell lines. Adult retinal pigment epithelial cell line-19 (ARPE-19) cells were genetically modified to either overexpress EMP2 (OE) or knock down EMP2 (KD) and expression at the RNA and protein level was evaluated using RNA sequencing and western blot respectively. Protein expression was evaluated under both normoxic conditions and conditions of hypoxic stress with 0.5% O2. EMP2 expression was found to positively correlate with expression of the pro-angiogenesis factors hypoxia inducible factor 1-alpha (HIF-1a) and VEGF for both RNA and protein. EMP2 mediated changes in ARPE-19 cells was also found to alter the secretion of a paracrine factor(s) in conditioned media that can regulate human umbilical vein endothelial cells (HUVEC) endothelial cell migration and capillary tube formation in in vitro functional angiogenesis assays. This study identifies EMP2 as a potentially important mediator of angiogenesis in the human RPE, a tissue involved in abnormal retinal neovascularization in a number of diseases. EMP2 levels positively correlate with those of the potent pro-angiogenesis mediators HIF-1a and VEGF, however the mechanism of this relationship remains to be clarified. This study supports further investigation of EMP2 as a promising novel target for therapeutic treatment of pathologic neovascularization in the retina.
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Project description:Transcriptional profiling to map the changes in placental function subsequent to maternal experimental UTI that result in intrauterine growth restriction.
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Project description:Intrauterine growth restriction (IUGR) represents a major obstetric challenge with perinatal complications and a risk factor of developing disease in adult life. Placental insufficiency is one of the common features accompanying IUGR. The aim of this study was to evaluate global placental gene expression profile in IUGR compared to normal pregnancies. Placental samples were collected by eight IUGR pregnancies with placental insufficiency ascertained by Doppler and eight healthy controls. A 30K Human Genome Survey Microarray v.2.0 (Applied Biosystems) was used to evaluate global gene expression profile. Principal component analysis showed good separation in terms of gene expression patterns between the groups. Pathway analysis with Bonferroni correction for multiple testing showed significant (p<0.05) up-regulation of inflammation mediated by chemokine and cytokine signalling pathway in the IUGR placentas. Genes involved in metabolism of glucocorticoids (HSD11B1 and DHRS2) were found differentially expressed. We found no imprinted genes to be differentially expressed and only one gene involved in epigenetic modifications (MBD3) to be down-regulated in the IUGR placentas, indicating that IUGR due to placental insufficiency is not associated to placental imprinting. Subgroup analysis between pure IUGR and IUGR with preeclampsia placentas showed only 27 differentially expressed genes suggesting common pathophysiology. Eight placental samples from normal human placenta compared to eight human placental samples from patients with intrauterine growth restrictions due to placental insufficiency
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Project description:The study objective was to determine differentially expressed mRNA transcripts in perirenal adipose tissue from fetal sheep that underwent sham or adrenal demedullation prior to fetal growth restriction to determine the role of catecholamines on gene expression following placental insufficiency-induced intrauterine growth restriction.
2023-12-05 | GSE132734 | GEO
Project description:Preeclampsia (PE) and Intrauterine Growth Restriction (IUGR) are major contributor of perinatal morbility and mortality, these pregnancy disorders associated with placental ischemia and share many similar pathophysiological features. The aim of this study was to compare the placental gene expression profiles including mRNA and lnRNAs from pregnant women from four study groups; PE, IUGR, PE-IUGR and normal pregnancy (NP). Gene expression microarray analysis was performed on placental tissue obtained at the moment of delivery and results were validated using RTq-PCR. Differential gene expression analysis revealed that the largest transcript variation was observed in the IUGR samples compared to NP (n=461; 314 mRNAs: 252 up-regulated and 62 down-regulated) and 133 lncRNAs: 36 up-regulated and 98 down-regulated). We also detected a group of differentially expressed transcripts shared between the PE and IUGR samples compared to NP (n=39), including 9 lncRNAs with a high correlation degree (P <0.05). Functional enrichment of these shared transcripts showed that cytokine signaling pathways, protein modification and regulation of JAK-STAT cascade are over-represented in both placental ischemic diseases. These findings contribute to the molecular characterization of placental ischemia showing common epigenetic regulation implicated in the pathophysiology of preeclampsia and Intrauterine Growth Restriction
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Project description:Transcriptional profiling to map the changes in placental function subsequent to maternal experimental UTI that result in intrauterine growth restriction. One condition experiment: 2 biological replicates of placenta from mice with maternal experimental UTI, 2 biological replicates of placenta from mice with sham UTI.
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Project description:The study objective was to determine differentially expressed mRNA transcripts in skeletal muscle from fetal sheep and 30 day old lambs to determine persistent gene changes following placental insufficiency-induced intrauterine growth restriction.
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