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Intrauterine growth restriction causes abnormal embyronic dentate gyrus neurogenesis in mouse offspring that leads to adult learning and memory deficits

ABSTRACT: In our mouse model of intrauterine growth restriction (IUGR), we have discovered that IUGR promotes embyronic Sox2+ neural stem cell depletion as well as premature neurogenesis. Using RNA-seq, we strived to determine the differentially expressed molecular genes/pathways that may be responsible for such cellular differences between appropriately-grown and IUGR mouse offspring.

ORGANISM(S): Mus musculus

PROVIDER: GSE173845 | GEO | 2021/09/15

REPOSITORIES: GEO

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Intrauterine growth restriction causes abnormal embyronic dentate gyrus neurogenesis in mouse offspring that leads to adult learning and memory deficits

Project description:Intrauterine growth restriction causes abnormal embyronic dentate gyrus neurogenesis in mouse offspring that leads to adult learning and memory deficits

| PRJNA727306 | ENA

Intrauterine Growth Restriction Causes Abnormal Embryonic Dentate Gyrus Neurogenesis in Mouse Offspring That Leads to Adult Learning and Memory Deficits.

Project description:Human infants who suffer from intrauterine growth restriction (IUGR), which is a failure to attain their genetically predetermined weight, are at increased risk for postnatal learning and memory deficits. Hippocampal dentate gyrus (DG) granule neurons play an important role in memory formation; however, it is unknown whether IUGR affects embryonic DG neurogenesis, which could provide a potential mechanism underlying abnormal postnatal learning and memory function. Using a mouse model of the most common cause of IUGR, induced by hypertensive disease of pregnancy, we first assessed adult learning and memory function. We quantified the percentages of embryonic hippocampal DG neural stem cells (NSCs) and progenitor cells and developing glutamatergic granule neurons, as well as hippocampal volumes and neuron cell count and morphology 18 and 40 d after delivery. We characterized the differential embryonic hippocampal transcriptomic pathways between appropriately grown and IUGR mouse offspring. We found that IUGR offspring of both sexes had short-term adult learning and memory deficits. Prenatally, we found that IUGR caused accelerated embryonic DG neurogenesis and Sox2+ neural stem cell depletion. IUGR mice were marked by decreased hippocampal volumes and decreased doublecortin+ neuronal progenitors with increased mean dendritic lengths at postnatal day 18. Consistent with its known molecular role in embryonic DG neurogenesis, we also found evidence for decreased Wnt pathway activity during IUGR. In conclusion, we have discovered that postnatal memory deficits are associated with accelerated NSC differentiation and maturation into glutamatergic granule neurons following IUGR, a phenotype that could be explained by decreased embryonic Wnt signaling.

| S-EPMC8503959 | biostudies-literature

Proteomic analysis of liver proteome affected by intrauterine growth restriction in newborn piglets.

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.

2016-03-15 | PXD003524 | Pride

RNA-sequencing data of liver tissue of intrauterine growth restricted (IUGR) piglets with or without supplementary energy treatment

Project description:RNA-sequencing data of liver tissue of intrauterine growth restricted (IUGR) piglets with or without supplementary energy treatment

2023-03-01 | GSE226052 | GEO

DNA Hypermethylation at Loci Associated with Diabetes, Obesity and Cardiac Abnormalities in CD3+ Lymphocytes of Intrauterine Growth Restricted Newbors

Project description:Intrauterine growth restriction (IUGR) is associated with increased susceptibility to obesity, metabolic syndrome and type 2 diabetes. Although the mechanisms underlying the fetal origin of metabolic disease are poorly understood, evidence suggests epigenomic alterations play a critical role. We sought to identify changes in DNA methylation patterns that define IUGR in CD3+ T-cells purified from umbilical cord blood obtained from appropriate for gestational age (Control) and IUGR male newborns using a genome-wide assay. We identified a global shift towards hypermethylation in IUGR compared to Control newborns targeted to regulatory regions of the genome.

2019-01-25 | GSE77268 | GEO

Effect of intrauterine growth restriction on fetal sex: biomarker discovery using cord blood plasma proteomics

Project description:Intrauterine growth restriction (IUGR) is associated with increased risk of cardiometabolic disease later in life and have been shown to affects female and male offspring differently, but the mechanisms remain unclear. The purpose of this study was to identify proteomic differences and metabolic risk markers in IUGR from male and female neonates when compare with appropriate for gestational age (AGA) that will provide a better understanding of IUGR pathogenesis and its associated risks. Our result revealed alterations in IUGR cord plasma proteomes with most of the enriched proteins implicated in peroxisome pathways. This effect was evident in females but not in males. Furthermore, we observed that catalase activity, peroxisome enzyme, was significantly increased in females (P<0.05) but unchanged in males. Finally, we identified risk proteins associated with obesity, type-2 diabetes, and glucose intolerance such as EGF containing fibulin extracellular matrix protein 1, proprotein convertase subtilisin/kexin type 9 (PCSK9) and transforming growth factor beta receptor 3 (TGFBR3) proteins unique to females while coagulation factor IX (C9) and retinol binding protein 4 (RBP4) are for males. Our data reveal that IUGR may display sexual dimorphism which may be associated with differences in lifelong risk for cardiometabolic disease between males and females.

2023-09-22 | PXD045578 | Pride

Sexually Dimorphic Response to Hepatic Injury in Newborn Suffering from Intrauterine Growth Restriction

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.

2024-01-31 | GSE222949 | GEO

Sexually Dimorphic Response to Hepatic Injury in Newborn Suffering from Intrauterine Growth Restriction

2024-01-31 | GSE233802 | GEO

Placental microarray profiling reveals common mRNA and lncRNA expression patterns in Preeclampsia and Intrauterine Growth Restriction

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

2020-05-31 | GSE147776 | GEO

BACE1 Deficiency Causes Abnormal Neuronal Clustering in the Dentate Gyrus.

Project description:BACE1 is validated as Alzheimer's ?-secretase and a therapeutic target for Alzheimer's disease. In examining BACE1-null mice, we discovered that BACE1 deficiency develops abnormal clusters of immature neurons, forming doublecortin-positive neuroblasts, in the developing dentate gyrus, mainly in the subpial zone (SPZ). Such clusters were rarely observed in wild-type SPZ and not reported in other mouse models. To understand their origins and fates, we examined how neuroblasts in BACE1-null SPZ mature and migrate during early postnatal development. We show that such neuroblasts are destined to form Prox1-positive granule cells in the dentate granule cell layer, and mainly mature to form excitatory neurons, but not inhibitory neurons. Mechanistically, higher levels of reelin potentially contribute to abnormal neurogenesis and timely migration in BACE1-null SPZ. Altogether, we demonstrate that BACE1 is a critical regulator in forming the dentate granule cell layer through timely maturation and migration of SPZ neuroblasts.

| S-EPMC5511112 | biostudies-literature

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