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An exploratory study to examine the effects of maternal choline supplementation during mouse pregnancy on placental epigenetic markers (miRNA-seq data set)

ABSTRACT: This study sought to explore the effects of 4X maternal choline supplementation (MCS) on mRNA and miRNA abundance in mouse placentas collected on gestational day 15.5. These data advance our understanding about the importance of choline in reproductive health and will guide future mechanistic studies designed to elucidate the mechanisms mediating choline's beneficial effects.

ORGANISM(S): Mus musculus

PROVIDER: GSE111295 | GEO | 2018/04/10

REPOSITORIES: GEO

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An exploratory study to examine the effects of maternal choline supplementation during mouse pregnancy on placental epigenetic markers (mRNA-seq data set)

Project description:This study sought to explore the effects of 4X maternal choline supplementation (MCS) on mRNA and miRNA abundance in mouse placentas collected on gestational day 15.5. These data advance our understanding about the importance of choline in reproductive health and will guide future mechanistic studies designed to elucidate the mechanisms mediating choline's beneficial effects.

2018-04-10 | GSE111294 | GEO

An exploratory study to examine the effects of maternal choline supplementation during mouse pregnancy on placental epigenetic markers

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-04-10 | GSE111296 | GEO

Basal forebrain cholinergic neurons are vulnerable in a mouse model of Down syndrome and their molecular fingerprint is rescued by maternal choline supplementation

Project description:Basal forebrain cholinergic neuron (BFCN) degeneration is a hallmark of Down syndrome (DS) and Alzheimer's disease (AD). Current therapeutics in these disorders have been unsuccessful in slowing disease progression, likely due to poorly understood complex pathological interactions and dysregulated pathways. The Ts65Dn trisomic mouse model recapitulates both cognitive and morphological deficits of DS and AD, including BFCN degeneration and has shown lifelong behavioral changes due to maternal choline supplementation (MCS). To test the impact of MCS on trisomic BFCN, we performed laser capture microdissection to individually isolate choline acetyltransferase-immunopositive neurons in Ts65Dn and disomic littermates, in conjunction with MCS at the onset of BFCN degeneration. We utilized single population RNA sequencing (RNA-seq) to interrogate transcriptomic changes within medial septal nucleus (MSN) BFCN. Leveraging multiple bioinformatic analysis programs on differentially expressed genes (DEGs) by genotype and diet, we identified key canonical pathways and altered physiological functions within Ts65Dn MSN BFCN, which were attenuated by MCS in trisomic offspring, including the cholinergic, glutamatergic and GABAergic pathways. We linked differential gene expression bioinformatically to multiple neurological functions, including motor dysfunction/movement disorder, early onset neurological disease, ataxia and cognitive impairment via Ingenuity Pathway Analysis. DEGs within these identified pathways may underlie aberrant behavior in the DS mice, with MCS attenuating the underlying gene expression changes. We propose MCS ameliorates aberrant BFCN gene expression within the septohippocampal circuit of trisomic mice through normalization of principally the cholinergic, glutamatergic, and GABAergic signaling pathways, resulting in attenuation of underlying neurological disease functions.

2023-10-30 | GSE246245 | GEO

Effects of maternal choline intake on placental gene expression

Project description:To explore the influence of maternal choline intake on placental gene expression, we employed whole genome microarray expression profiling to identify genes that were differentially expressed in placental tissues obtained from women consuming two different doses (480 vs. 930 mg/d) of choline throughout the third trimester of pregnancy. Healthy third trimester (gestational week 26-29) pregnant women were randomized to a 12-week choline controlled feeding study. The participants consumed either 480 (n=6) or 930 (n=6) mg choline/d. Full thickness placental samples were collected at delivery to extract RNA and perform the arrays. Healthy third trimester (gestational week 26-29) pregnant women were randomized to a 12-week choline controlled feeding study. The participants consumed either 480 (n=6) or 930 (n=6) mg choline/d for 12 weeks. Placental samples were obtained at delivery

2012-07-12 | E-GEOD-39290 | biostudies-arrayexpress

An exploratory study to examine the effects of maternal choline supplementation during mouse pregnancy on placental epigenetic markers

Project description:An exploratory study to examine the effects of maternal choline supplementation during mouse pregnancy on placental epigenetic markers

| PRJNA436481 | ENA

Effects of maternal choline intake on placental gene expression

2012-07-13 | GSE39290 | GEO

Maternal Choline Supplementation during Normal Murine Pregnancy Alters the Placental Epigenome: Results of an Exploratory Study.

Project description: Not available

| S-EPMC5946202 | biostudies-literature

An exploratory study to examine the effects of maternal choline supplementation during mouse pregnancy on placental epigenetic markers (mRNA-seq data set)

Project description:An exploratory study to examine the effects of maternal choline supplementation during mouse pregnancy on placental epigenetic markers (mRNA-seq data set)

| PRJNA436482 | ENA

An exploratory study to examine the effects of maternal choline supplementation during mouse pregnancy on placental epigenetic markers (miRNA-seq data set)

Project description:An exploratory study to examine the effects of maternal choline supplementation during mouse pregnancy on placental epigenetic markers (miRNA-seq data set)

| PRJNA436483 | ENA

Transcriptional profiling of mouse liver tissue following control, choline and methonine/choline deficient diet intervention

Project description:Choline and methionine/choline deficient diets are widely used to generate severe rodent hepatic steatosis and steatohepatitis in an attempt to reflect stages of human non-alcoholic fatty liver disease (NAFLD). The underlying mechanism of hepatic injury in these models, and how this reflects human disease remains incompletely understood. We used detailed transcriptional analysis to interrogate the molecular mechanisms of this intervention and its similarity to human disease. Adult C57Bl/6J mice were maintained on control, choline deficient (CDD) or methionine/choline deficient (MCDD) diets for 4 weeks. Isolated liver RNA was used for transcriptional profiling by micro array analysis.

2016-06-01 | E-MTAB-3943 | biostudies-arrayexpress

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