Folic acid intake during juvenile/peri-pubertal development modulates the mammary tissue transcriptome of female C56BL/6 mice
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ABSTRACT:
PROVIDER: PRJNA789906 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17263800_1.fastq.gz | Fastqsanger.gz | |||
| SRR17263800_2.fastq.gz | Fastqsanger.gz | |||
| SRR17263801_1.fastq.gz | Fastqsanger.gz | |||
| SRR17263801_2.fastq.gz | Fastqsanger.gz | |||
| SRR17263802_1.fastq.gz | Fastqsanger.gz |
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Project description:We tested the hypothesis that high FA (HFA) intake alters the juvenile/peri-pubertal mammary transcriptome in a manner consistent with increased potential for breast cancer, detectable beyond the period of intake. C57BL/6 mice were fed control FA (CFA) (1 mg/kg diet) or HFA (5 mg/kg diet) diets for 4 weeks, followed by AIN93M maintenance diet for 4 weeks. RNA sequencing of the mammary transcriptome (~83 million reads) showed 18 transcripts (17 downregulated) differentially expressed between groups. Gene Set Enrichment showed downregulated genes significantly enriched in oxidative phosphorylation, adipogenesis, fatty acid metabolism and epithelial mesenchymal transition. Cancer and developmental disorder were the most altered Disease and Disorder pathways, with top upstream regulators identified as DNA methyltransferases. This study demonstrates HFA intake during juvenile/peri-pubertal mammary development induces changes in the mammary transcriptome associated with altered energy metabolism, cell neoplasia and epigenetic regulation of gene.
2024-12-01 | GSE191160 | GEO
Project description:There is a lack of systematic investigations of large-scale transcriptome patterns associated with normal breast development. Herein, we profiled whole-transcriptome (by microarrays) of normal mammary glands in female Sprague-Dawley rats, an animal model widely used in breast cancer research, across six distinctive developmental stages – pre-pubertal, peri-pubertal, pubertal, lactation, and adult parous and age-matched nulliparous.
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Project description:Purpose: To identify, using RNA-sequencing, differentially expressed genes in the mammary gland of mice supplemented with FA. We aimed to ascertain whether gene expression is persistently altered after increased FA supplementation, whether such alterations are related to genes implicated in epigenetic regulation and disease risk. Methods: Mammary gland mRNA profiles of mice 4 weeks after folic acid supplementation (5mg/kg vs 1mg/kg) during adulthood were generated by deep sequencing using RNA sequencing. The sequence reads that passed quality filters were aligned to the mouse genome using TopHat and analyzed at the gene level using DESeq2. qRT–PCR validation was performed using SYBR Green assays Results: Using an optimized data analysis workflow, we mapped reads to the mouse genome (build mm10) and identified 222 genes differentially expressed between the two group (adjsuted p value <0.05). 191 of these were upregulated and 31 were downregulated. Geneset enrichment analysis identified several enriched pathways, including epithelial mesenchymal transition and myogenesis. Conclusions: Our study provides novel insights into the persistent effects of FA intake on the C57BL/6 mammary transcriptome and identifies putative gene targets and molecular pathways that help to understand how increasing FA intake may modulate the long term expression of gene networks and disease pathways.
2020-09-15 | GSE153732 | GEO
Project description:Background: The exact nature of the interrelationship between pubertal brain development and hormones involvement has always attracted wide interest. Brain structural changes that occur during the pubertal developmental process mainly appear in the regions most closely linked with emotion, motivation and cognitive functions. Using a sheep model, we have previously shown that peri-pubertal pharmacological blockade of gonadotropin-releasing hormone (GnRH) receptors results in increased sex-differences in cognitive executive function and emotional control, as well as in a sex- and side-specific gene expression pattern of hippocampal genes associated with synaptic plasticity and endocrine signaling. In this study, we explore the effects of this treatment regime on the amygdalar gene expression profile. Methods: The study was conducted with 30 same-sex twin lambs (14 female and 16 male), half of which were treated with the GnRH agonist (GnRHa) goserelin acetate every 4th week, beginning before puberty, until 50 weeks of age. The gene expression profiles of left and right amygdala samples from all 30 animals were measured by using ovine 8 X 15 K Agilent microarrays. Furthermore, differential expression of a selected number of genes was confirmed by qRT-PCR (Quantitative real time PCR). Networking analyses and Gene Ontology (GO) Term analyses were performed with the Ingenuity Pathway Analysis (IPA), version 7.5 DAVID (Database for Annotation, Visualization and integrated Discovery) software packages respectively. Results: GnRHa treatment was associated with significant sex- and hemisphere-specific differential expression of genes. Interestingly, genome-wide transcription showed a set of 438 (p value <0.05) genes in female treated left and 46 (p value <0.0.5) genes in females treated right amygdala were differentially expressed but not in any treatment group of male animals. Conclusion: Our results indicate that GnRH directly and/or indirectly is involved in the regulation of sex- and side-specific differential expression of genes in amygdala. Hence, this finding should be considered when long-term peri-pubertal GnRHa treatment is used in children.
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Project description:Dietary fat consumption during rapid mammary gland developing period such as peri-pubertal maturation or pregnancy increases the risk for breast cancer. However, the molecular mechanism underlying this observation is not well elucidated. To provide mechanistic insight, we examined gene expression profile in mouse mammary epithelial cells (MMECs) exposed to high-fat diet (HFD) or control diet (CD). Trp53-/- female mice were treated with experimental diets for 5 weeks during the peri-puberty period (3 to 8 weeks of age). This treatment induced insignificant difference in body weight between mice exposed to HFD and CD. Gene Set Enrichment Analysis (GSEA) predicted elevated expression of c-Myc target genes when exposed to HFD. Consistently, we detected marked elevation of c-Myc protein and prolongation of its half-life in MMECs exposed to HFD suggesting that HFD increased its stability. Additionally, we observed increased phosphorylation at c-MycS62 with concomitant increase in ERK phosphorylation. HFD rendered Trp53-/- MMECs more colonogenic and spherogenic, which was antagonized by a c-Myc inhibitor. Oleic acid the main fatty acid constituent of the HFD and TAK-875 an agonist for G protein-coupled receptor 40 (a receptor for oleic acid) as well enhanced c-Myc stabilization and MMECs proliferation. Collectively, these data suggest that HFD exerts its effect on MMECs through the stabilization of an oncoprotein, deciphering a novel mechanism whereby dietary fat promotes mammary carcinogenesis.
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Project description:Peri-pubertal High-Fat Diet Promotes c-Myc Stabilization in Mammary Gland Epithelium
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Project description:Transcriptomic evaluation of bovine embryo quality on blastocysts obtained from peri-pubertal oocyte donors
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Project description:Peri- and post-pubertal estrogen exposures of female mice optimize uterine responses later in life
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Project description:At birth, all female mice, including those that either lack estrogen receptor α (ERα-knockout) or that express mutated forms of ERα (AF2ERKI), have a hypoplastic uterus. However, uterine growth and development that normally accompanies pubertal maturation does not occur in ERα-knockout or AF2ERKI mice, indicating ERα mediated estrogen signaling is essential for this process. Mice that lack Cyp19 (aromatase, ArKO mice), an enzyme critical for estrogen (E2) synthesis, are unable to make E2, and lack pubertal uterine development. A single injection of E2 into ovariectomized adult (10 weeks old) females normally results in uterine epithelial cell proliferation, however, we observe that, although ERα is present in the ArKO uterine cells, no proliferative response is seen. We assessed the impact of exposing ArKO mice to E2 during pubertal and post-pubertal windows and observed that E2 exposed ArKO mice acquired growth responsiveness. Analysis of differential gene expression between unexposed ArKO samples and samples from animals exhibiting the ability to mount an E2-induced uterine growth response (WT or E2 exposed ArKO) revealed activation of EZH2 and HAND2 signaling and inhibition of GLI1 responses. EZH2 and HAND2 are known inhibit uterine growth, and GLI1 is involved in IHH signaling, which is a positive mediator of uterine response. Finally, we show that exposure of ArKO females to dietary phytoestrogens results in their acquisition of uterine growth competence. Altogether our findings suggest that pubertal levels of endogenous and exogenous estrogens impact biological function of uterine cells later in life via ERα-dependent mechanisms. We compared uterine RNA from ovariectomized adult aromatase knockout mice (ARKO) mice that were untreated to WT mice and to ARKO that were administered estradiol benzoate (EB) to induce uterine epithelial cell growth competence
2020-04-29 | GSE147900 | GEO
Project description:Folic acid is present in pre-natal vitamins, fortified cereal grains and multi-vitamin supplements. High intake of folic acid through these sources has resulted in populations with increased levels of serum folate and unmetabolized folic acid. Although the benefits of folic acid in the prevention of neural tube defects are undeniable, the impact of long-term consumption of folic acid on the prostate is not fully understood. In this study, we used a rodent model to test whether dietary folic acid (FA) supplementation changes prostate homeostasis and response to androgen deprivation. Although intact prostate weights do not differ between diet groups, we made the surprising observation that dietary folic acid supplementation confers partial resistance to castration-mediated prostate involution. More specifically, male mice that were fed a folic acid supplemented diet and then castrated had greater prostate wet weights, greater prostatic luminal epithelial cell heights, and more abundant RNAs encoding prostate secretory proteins compared to mice that were fed a control diet and castrated. We used RNA-seq to identify signaling pathways enriched in the castrated prostates from folic acid supplemented diet fed mice compared to control mice. We observed differential expression of genes involved in several metabolic pathways in the FA supplemented mice. Together, our results show that dietary FA supplementation can impact metabolism in the prostate and attenuate the prostate’s response to androgen deprivation. This has important implications for androgen deprivation therapies used in the treatment of prostate disease, as consumption of high levels of folic acid could reduce the efficacy of these treatments.
2018-08-22 | GSE116299 | GEO