Sus scrofa breed:Landrace
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA420637 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6339840.fastq.gz | Fastqsanger.gz | |||
| SRR6339840_1.fastq.gz | Fastqsanger.gz | |||
| SRR6339840_2.fastq.gz | Fastqsanger.gz | |||
| SRR6339850.fastq.gz | Fastqsanger.gz | |||
| SRR6339850_1.fastq.gz | Fastqsanger.gz |
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Project description:Poor maternal nutrition during pregnancy causes intrauterine growth retardation, which, in turn, is associated with increased risk of cardiovascular and metabolic diseases in later life Fetal hearts were collected from baboon fetuses born to regularly fed and undernurished mothers. Total RNA was isolated, and fetal cardiac miRNA were profiled
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Project description:Fetal growth in utero is affected by both inherent genetic programming in combination with environmental factors, such as maternal health and nutrition. Epidemiologic data in growth-altered fetuses, either growth-restricted (IUGR) or large for gestational age (LGA), demonstrate compelling evidence that these fetuses are at increased risk for cardiovascular and metabolic disease in adulthood. In this study, we used RRBS to examine genome wide DNA methylation variation in placental samples from offspring born IUGR, LGA, and appropriate for gestational age (AGA). We identified almost 200 differentially methylated genes among these groups. Among these genes, the differentially methylated regions were disproportionately located in transcription-regulatory regions such as promoters. Our results suggest that the gene expression and methylation state of the human placenta are related and sensitive to the intrauterine environment. We profiled DNA methylation for 17 human placentas, in which 5 were from LGA, 6 from IUGR and 6 from AGA placentas as controls
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Project description:Impaired muscle growth as a result of IUGR is a major contributor to lifelong reductions in muscle mass (sarcopenia) and metabolic disease risk. We use an ovine model of chronic placental insufficiency which restricts nutrient supply from mother to fetus and results in intrauterine growth restriction. In our model of placental insufficiency and IUGR, fetal hindlimb muscles weigh less than normally-grown control fetuses and have smaller myofiber diameters. Given the frequent correlation between functional changes and transcriptional changes, we investigated the effect of chronic placental insufficiency and IUGR on fetal skeletal muscle gene expression. We found that gene expression in the skeletal muscle is significantly altered by chronic placental insufficiency. In gene ontology analysis, we found that genes involved in cell cycle regulation were most significantly affected, with downregulation of several cyclins. These observations may in part account for decreased muscle weight relative to brain weight observed in the late gestation IUGR fetus.
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Project description:Intrauterine growth restriction (IUGR) impairs fetal growth and development, perturbs nutrient metabolism, and increases the risk of developing diseases in the postnatal life. However, the underlying mechanisms by which IUGR affects fetuses remain incompletely understood. Here, we applied high-throughput proteomics approach and biochemical analysis to investigate the impact of IUGR on fetal liver.
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Project description:Breast milk has shown neurodevelopmental advantages compared to infant formula, especially in IUGR infants, which may relate to the fat source. This study aimed to compare neurodevelopmental outcomes in normal birth weight (NBW) and intrauterine growth restricted (IUGR) piglets fed a formula diet with either a vegetable oil (VEG) or bovine milk fat source (MILK). Results showed that total plasma lipids were increased by feeding the MILK diet. 82% and 11% of lipid species were differentially expressed between dietary groups in plasma and hippocampus, respectively, with slight agreement between the plasma and brain lipidome. The MILK diet was most effective in increasing brain lipid accretion, mainly comprising phospholipids. Absolute regional brain weights, grey and white matter volumes, and behavior and motor function scores were lower in IUGR piglets with no effects of diet. Cognitive function and gene expression profiles were similar for dietary and weight groups, and overall only minor interactive effects between diet and weight were observed. In conclusion, dietary fat source influenced the plasma and to a lesser degree the hippocampal lipidome, but was unable to improve on IUGR induced brain structural and functional impairments.
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Project description:Intrauterine growth restriction (IUGR) is associated with increased relative liver weight at birth, hepatic function decline, and a higher risk for chronic liver and cardiovascular diseases in adults. Precise mechanisms of early developmental plasticity to intervene in poor fetal programming and adult disease remain largely elusive and warrant extensive research. Selecting natural piglets’ model of IUGR, using the liver as a readout and combining previous transcriptome findings, a map of cellular landscape was created to reveal a sex-dependent manner in IUGR-induced hepatic injury and its long-term functional repercussions.Here, we show data on the transcriptional profiles of 41,969 high-quality cells from normal birthweight (NBWs) and IUGR piglets (IUGRs) from hepatic tissue and demonstrated strong homology with human using human-derived liver single-cell dataset. We discovered that male liver was much more severely damaged and inflammation by IUGR than female liver at the one-week postnatal node.
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Project description:Epidemiological data indicated intrauterine growth retardation (IUGR) is a risk factors for adult metabolic syndrome. However, the genetic mechanism underlying the phenotype in adulthood is not well characterized. Here, the present study employed adult normal and IUGR pigs as models to survey the difference of global gene expression in the liver using transcriptome sequence. The trancriptome libraries generated 104.54 gigabases data, 16,948 and 17,078 genes were expressed in normal and IUGR pigs, repectively. A total of 1,322 differentially expreesion genes (DGEs) were identified. An enrichment analysis of DGEs presented the top overrepresented GO terms and pathway were related to oxidoreductase activity, ATPase activity, amino catabolic process, glucose metabolism and Insulin signaling pathway. Finally, combined their phenotypes and gene expression patterns, we proved the adult IUGR pigs would obstruct the process of mitochondrial biogenesis and oxidative phosphorylation, which induced high oxidation press in adult IUGR. The increased gluconeogenic and decreased glycogen synthesis in liver resulted in reducing the capacity of glucose intolerance in IUGR. The decreased expression of insulin signaling genes (such as PI3K and AKT) implied a risk of diabetes in adult IUGR. Moreover, the capacity of fatty acid oxidation decreased in IUGR liver leaded to high content of triglyceride and free fatty acid in IUGR. Together, these findings provide a comprehensive understanding of the molecular mechanisms of adult IUGR pigs and valuable information for future studies of therapeutic intervention in IUGR metabolic syndrome.
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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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