Identification and Comparative Analyses of Myocardial miRNAs Involved in Fetal Response to Maternal Undernutrition
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ABSTRACT:
ORGANISM(S): Papio hamadryas
PROVIDER: GSE69609 | GEO | 2015/11/02
SECONDARY ACCESSION(S): PRJNA285981
REPOSITORIES: GEO
Similar Datasets
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
2015-11-02 | E-GEOD-69609 | biostudies-arrayexpress
Project description:Maternal obesity programs the offspring to cardiovascular disease, insulin resistance, and obesity. We sequenced and profiled the cardiac miRNAs that were dysregulated in the hearts of baboon fetuses born to a high fat / high fructose diet fed mothers compared to a regular diet fed mothers. Fetal hearts were collected from baboon fetuses born to obese and lean mothers, total RNA was isolated, and fetal cardiac miRNA were sequenced and profiled
2013-02-01 | E-GEOD-43323 | biostudies-arrayexpress
Project description:Maternal obesity programs the offspring to cardiovascular disease, insulin resistance, and obesity. We sequenced and profiled the cardiac miRNAs that were dysregulated in the hearts of baboon fetuses born to a high fat / high fructose diet fed mothers compared to a regular diet fed mothers.
2013-02-01 | GSE43323 | GEO
Project description:Human and animal studies show that suboptimal intrauterine environments lead to fetal programming, predisposing offspring to disease in later life. Maternal obesity has been shown to program offspring for cardiovascular disease (CVD), diabetes, and obesity. MicroRNAs (miRNAs) are small, noncoding RNA molecules that act as key regulators of numerous cellular processes. Compelling evidence links miRNAs to the control of cardiac development and etiology of cardiac pathology; however, little is known about their role in the fetal cardiac response to maternal obesity. Our aim was to sequence and profile the cardiac miRNAs that are dysregulated in the hearts of baboon fetuses born to high fat/high fructose-diet (HFD) fed mothers for comparison with fetal hearts from mothers eating a regular diet. Eighty miRNAs were differentially expressed. Of those, 55 miRNAs were upregulated and 25 downregulated with HFD. Twenty-two miRNAs were mapped to human; 14 of these miRNAs were previously reported to be dysregulated in experimental or human CVD. We used an Ingenuity Pathway Analysis to integrate miRNA profiling and bioinformatics predictions to determine miRNA-regulated processes and genes potentially involved in fetal programming. We found a correlation between miRNA expression and putative gene targets involved in developmental disorders and CVD. Cellular death, growth, and proliferation were the most affected cellular functions in response to maternal obesity. Thus, the current study reveals significant alterations in cardiac miRNA expression in the fetus of obese baboons. The epigenetic modifications caused by adverse prenatal environment may represent one of the mechanisms underlying fetal programming of CVD.
| S-EPMC3798778 | biostudies-literature
Project description:Intra-uterine growth restriction (IUGR) and fetal overgrowth increase the risk of postnatal health. Maternal nutrition is the major intrauterine environmental factor that alters fetal weight. However, the mechanisms underlying maternal nutrition affect fetal development is not entirely clear. We developed a pig model and used isobaric tags for relative and absolute quantification (iTRAQ) to investigate alterations in the placental proteome were obtained from gilts in normal-energy-intake (Con) and high-energy-intake (HE) group, respectively.At 90 d of gestation, the heavy fetuses were found at the tubal ends and light fetuses at the cervical ends of the uterus in Con group and the heavy fetuses had higher glucose concentration than the light fetuses. However, a higher uniformity was noted in HE group. Placental promote between these two positions indicated that a total of 78 and 50 differentially expressed proteins were detected in Con and HE group, respectively. In Con group, these proteins related to lipid metabolism (HADHA, AACS, CAD), nutrient transport (GLUT, SLC27A1) and energy metabolism (NDUFV1, NDUFV2, ATP5C1). However, the differentially expressed proteins in HE group were mainly participation in transcriptional and translational regulation and intracellular vesicular transport.
2018-10-26 | PXD004951 | Pride
Project description:Poor maternal nutrition causes intrauterine growth restriction (IUGR); however, its effects on fetal cardiac development are unclear. We have developed a baboon model of moderate maternal undernutrition, leading to IUGR. We hypothesized that the IUGR affects fetal cardiac structure and metabolism. Six control pregnant baboons ate ad-libitum (CTRL)) or 70% CTRL from 0.16 of gestation (G). Fetuses were euthanized at C-section at 0.9G under general anesthesia. Male but not female IUGR fetuses showed left ventricular fibrosis inversely correlated with birth weight. Expression of extracellular matrix protein TSP-1 was increased (p<0.05) in male IUGR. Expression of cardiac fibrotic markers TGFß, SMAD3 and ALK-1 were downregulated in male IUGRs with no difference in females. Autophagy was present in male IUGR evidenced by upregulation of ATG7 expression and lipidation LC3B. Global miRNA expression profiling revealed 56 annotated and novel cardiac miRNAs exclusively dysregulated in female IUGR, and 38 cardiac miRNAs were exclusively dysregulated in males (p<0.05). Fifteen (CTRL) and 23 (IUGR) miRNAs, were differentially expressed between males and females (p<0.05) suggesting sexual dimorphism, which can be at least partially explained by differential expression of upstream transcription factors (e.g. HNF4a, and NF?B p50). Lipidomics analysis of fetal cardiac tissue exhibited a net increase in diacylglycerol and plasmalogens and a decrease in triglycerides and phosphatidylcholines. In summary, IUGR resulting from decreased maternal nutrition is associated with sex-dependent dysregulations in cardiac structure, miRNA expression, and lipid metabolism. If these changes persist postnatally, they may program offspring for higher later life cardiac risk.
2018-04-30 | MTBLS426 | MetaboLights
Project description:Suboptimal intrauterine nutrition predisposes the fetus to central obesity and metabolic syndrome in adult life, suggesting nutritional programming of the fat distribution. However, the underlying mechanisms are not elucidated. We hypothesized that prenatal nutritional deprivation leads to stimulation of adipogenesis, as an adaptive mechanism, in a depot-dependent manner. The induction of adipogenesis is most enhanced in the subcutaneous lower-body depots, followed by the subcutaneous upper-body and visceral adipose tissue depots. Stimulation of adipogenesis may lead to an early consumption of the stem cell pool, and thus, may impair adipose tissue expandability postnatally, which may lead to differences in regional adipose tissue growth. We tested this hypothesis by analyzing global gene expression to identify expression patterns in subcutaneous abdominal, subcutaneous femoral, and omental adipose depots of baboon fetuses that have been altered by nutritional maternal deprivation. Adipose tissue was collected from baboon fetuses at 165 dG from mothers fed control or 30% nutrient-restricted diets (three females and one male in each group). 24 samples, each consisted of pooled total RNA from triplicate wells (6-well plate).
2011-12-16 | E-GEOD-34464 | biostudies-arrayexpress
Project description:Suboptimal intrauterine nutrition predisposes the fetus to central obesity and metabolic syndrome in adult life, suggesting nutritional programming of the fat distribution. However, the underlying mechanisms are not elucidated. We hypothesized that prenatal nutritional deprivation leads to stimulation of adipogenesis, as an adaptive mechanism, in a depot-dependent manner. The induction of adipogenesis is most enhanced in the subcutaneous lower-body depots, followed by the subcutaneous upper-body and visceral adipose tissue depots. Stimulation of adipogenesis may lead to an early consumption of the stem cell pool, and thus, may impair adipose tissue expandability postnatally, which may lead to differences in regional adipose tissue growth. We tested this hypothesis by analyzing global gene expression to identify expression patterns in subcutaneous abdominal, subcutaneous femoral, and omental adipose depots of baboon fetuses that have been altered by nutritional maternal deprivation. Adipose tissue was collected from baboon fetuses at 165 dG from mothers fed control or 30% nutrient-restricted diets (three females and one male in each group).
2011-12-16 | GSE34464 | GEO
Project description:Undernutrition during pregnancy is implicated in the programming of offspring for the development of obesity and diabetes. We hypothesized that maternal programming causes epigenetic changes in fetal hypothalamic pathways regulating metabolism. This study used sheep to examine the effect of moderate maternal undernutrition (60 d before to 30 d after mating) and twinning to investigate changes in the key metabolic regulators proopiomelanocortin (POMC) and the glucocorticoid receptor (GR) in fetal hypothalami. Methylation of the fetal hypothalamic POMC promoter was reduced in underfed singleton, fed twin, and underfed twin groups (60, 73, and 63% decrease, respectively). This was associated with reduced DNA methyltransferase activity and altered histone methylation and acetylation. Methylation of the hypothalamic GR promoter was decreased in both twin groups and in maternally underfed singleton fetuses (52, 65, and 55% decrease, respectively). This correlated with changes in histone methylation and acetylation and increased GR mRNA expression in the maternally underfed singleton group. Alterations in GR were hypothalamic specific, with no changes in hippocampi. Unaltered levels of OCT4 promoter methylation indicated gene-specific effects. In conclusion, twinning and periconceptional undernutrition are associated with epigenetic changes in fetal hypothalamic POMC and GR genes, potentially resulting in altered energy balance regulation in the offspring.
| S-EPMC3316895 | biostudies-other
Project description:Maternal nutrition during embryonic development and lactation influences multiple aspects of offspring health. Using mice, this study investigates the effects of maternal caloric restriction (CR) during mid-gestation and lactation on offspring neonatal development and on adult metabolic function when challenged by a high fat diet (HFD). The CR maternal model produced male and female offspring that were significantly smaller, in terms of weight and length, and females had delayed puberty. Adult offspring born to CR dams had a sexually dimorphic response to the high fat diet. Compared to offspring of maternal control dams, adult female, but not male, CR offspring gained more weight in response to high fat diet at 10 weeks. In adipose tissue of male HFD offspring, maternal undernutrition resulted in blunted expression of genes associated with weight gain and increased expression of genes that protect against weight gain. Regardless of maternal nutrition status, HFD male offspring showed increased expression of genes associated with nonalcoholic liver disease (NAFLD). Furthermore, we observed significant, sexually dimorphic differences in serum TSH. These data reveal tissue- and sex-specific changes in gene and hormone regulation following mild maternal undernutrition, which may offer protection against diet induced weight gain in adult male offspring.
2024-01-04 | GSE247985 | GEO