Genome wide anaylsis of rats exposed to endocrine disruptors.
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PROVIDER: PRJNA540251 | ENA |
REPOSITORIES: ENA
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Project description:Genome wide anaylsis of transcriptome modifications in rats exposed to endocrine disruptors. [RNA-Seq]
| PRJNA540257 | ENA
Project description:Genome wide anaylsis of histone modifications in rats exposed to endocrine disruptors. [ChIP-Seq]
| PRJNA540150 | ENA
Project description:Environmental reproductive health focuses on the effect of exposure to contaminants considered as endocrine disruptors. Developmental testis is considered as target of these compounds affecting testicular functions in adults and suspected implications in tumor etiology. Comparative analysis of gene expression in mouse testis exposed to five disruptors, three different dosages and three accumulative developmental stages shown defined signature profiles of gene deregulation for MEHP (monoethyl phthalate) and zearalenone (a phytoestrogen) and different to 17β-estradiol exposure. The effects are even detected in postpuberal male offspring from premating exposed mothers. Oxidative stress response, protein ubiquitination and oxidative phosphorylation are the most representative pathways affected.
2010-06-01 | GSE14774 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2020-03-11 | GSE130436 | GEO
Project description:Our early life environment has a profound influence on developing organs and tissues that impacts metabolic function, and determines health and disease susceptibility across the life-course. We show an adverse early-life exposure that causes metabolic dysfunction in adulthood reprograms active and repressive histone marks in the developing liver to accelerate acquisition of an adult epigenomic signature at specific genes and chromatin states. This epigenomic reprogramming persists long after the initial exposure, but remarkably, can remain transcriptionally- and metabolically-silent until later-life exposure to a Western-style (high fat-fructose-cholesterol) diet. These findings reveal the importance of epigenome:environment interactions across the life-course, which early in life accelerate epigenomic aging and reprogram the epigenome, and later in adulthood, can unlock metabolically restriced epigenetic reprogramming to drive metabolic dysfunction.
2020-03-11 | GSE130434 | GEO
Project description:Our early life environment has a profound influence on developing organs and tissues that impacts metabolic function, and determines health and disease susceptibility across the life-course. We show an adverse early-life exposure that causes metabolic dysfunction in adulthood reprograms active and repressive histone marks in the developing liver to accelerate acquisition of an adult epigenomic signature at specific genes and chromatin states. This epigenomic reprogramming persists long after the initial exposure, but remarkably, can remain transcriptionally- and metabolically-silent until later-life exposure to a Western-style (high fat-fructose-cholesterol) diet. These findings reveal the importance of epigenome:environment interactions across the life-course, which early in life accelerate epigenomic aging and reprogram the epigenome, and later in adulthood, can unlock metabolically restriced epigenetic reprogramming to drive metabolic dysfunction.
2020-03-11 | GSE130409 | GEO
Project description:Environmental reproductive health focuses on the effect of exposure to contaminants considered as endocrine disruptors. Developmental testis is considered as target of these compounds affecting testicular functions in adults and suspected implications in tumor etiology. Comparative analysis of gene expression in mouse testis exposed to five disruptors, three different dosages and three accumulative developmental stages shown defined signature profiles of gene deregulation for MEHP (monoethyl phthalate) and zearalenone (a phytoestrogen) and different to 17β-estradiol exposure. The effects are even detected in postpuberal male offspring from premating exposed mothers. Oxidative stress response, protein ubiquitination and oxidative phosphorylation are the most representative pathways affected. Animal Exposure CD-1 mice were in vivo exposed to several doses of EDs following a defined protocol: mothers were exposed two weeks before mating (exposure A); the same exposure and dose were maintained during pregnancy (exposure B) and four weeks after birth (exposure C). In all exposures, male offspring were sacrificed to obtain the testes. The compounds were administrated in drinking water to a final concentration of: E2(mg/l) BPA(mg/l) Zea(mg/l) MEHP(mg/l) Lindane(mg/l) Dose (1) 0.02 0.5 4 27.85 50 Dose (2) 0.04 50 12 139.17 100 Dose (3) 0.16 200 20 278.34 200 Ethanol was used as vehicle for E2, BPA and Zea and DMSO was for MEHP and Lindane. Control testes were obtained from animals exposed to solvents of EDs: Ethanol and DMSO. Animal care and sacrifice were made following regulations from the CSIC Bioethics Committee. RNA preparation Total RNA from testes of exposed animals and controls was extracted using TRIzol reagent (Invitrogen), according to the manufacturer’s standard protocol. RNA samples were spectrophotometrically quantified using NanoDrop (NanoDrop Technologies). To minimize the effect of inter-individual expression variability we made pools of RNA from at least 3 individual RNA samples from each experimental condition (same quantity of total RNA per sample). Pools of RNA were checked for quality performing Experion analysis (Bio-Rad Laboratories). Total RNA from testes of unexposed four weeks old animals was also extracted with the purpose of making pools to assess the variability at the expression level of the mouse strain used (Ctr). Microarray Processing Starting with total RNA from pools described above, full length cDNAs were synthesized from oligo(dT) primers bearing a T7 promoter. These cDNAs were used as template for in vitro transcription by T7-RNA-Polymerase to amplify the mRNAs; following the Amino Allyl MessageAmp™ aRNA Kit (Ambion, Inc.) protocol. The amplified mRNAs (aRNA) were labeled either with Cy3 or Cy5 dyes, using Amersham CyDye Post-Labeling Reactive Dyes (Amersham Biosciences). The incorporated dye was spectrophotometrically quantified using NanoDrop (NanoDrop Technologies). The same dye signal quantities of labeled experimental and control aRNAs were mixed and hybridized to Mouse Oligoset v3 (OPERON) arrays from Genomics facility-University of Cincinnati (USA). The slides contained 31,769 spotted probes (70 mer oligonucleotides) corresponding to 24,878 expressed or predicted mouse genes. Hybridization and washes of microarrays were performed according to Genomics facility-University of Cincinnati instructions. Dye-Swap replicates were performed: one slide hybridized with experimental and control targets labeled with Cy3 and Cy5, respectively; and the second slide with the same type of targets but inversely labeled. Target refers to labeled aRNA while probe refers to the oligonucleotides spotted on the microarray platform. Imaging and data generation were carried out using a GenePix 4000B (Axon Instruments) and associated software from Axon Instruments, Inc. The microarray slides were scanned with dual lasers with wavelength frequencies to excite Cy3 and Cy5. Images were captured in TIFF files. Information extraction for a given spot was based on the median value for the signal pixels minus the median value for the background pixels to produce a gene set data file for all the DNA spots. The Cy3 and Cy5 fluorescence signal intensities were normalized.
2010-06-01 | E-GEOD-14774 | biostudies-arrayexpress
Project description:Purpose: In testis the effects of exposure to mixtures of Endocrine disruptors compounds (EDCs) upon expression of miRNAs were not addressed. Objective: To identify the expression profiles of the 'miRNome' in mice testis chronic exposed to a defined mixture of five EDCs. Methods: Pregnant mice from 0.5 post-coital day were exposed in the drinking water to a mixture containing 0.3 mg/Kg-bw/day of each phthalate (DEHP, DBP, BBP), plus 0.05 mg/Kg-bw/day of each alkylphenol (NP, OP) until adulthood of male mouse (60 days old). We characterized the 'miRNome' by next generation sequence (NGS). Results: In mouse testis exposed to EDCs mixture we detected by NGS 2 up-regulated and 8 down-regulated miRNAs along to 36 isomiRs differentially expressed; these results were validated by RT-qPCR. and functional analysis showed deregulation of testicular hormonal status, spermatogenesis disruption and germ cells apoptosis. Conclusions: Here we provide the first association between deregulation of miRNAs, isomiRs, with histopathological and hormonal alterations in adult mice testis exposed to mixture of EDCs.
2017-07-31 | GSE84695 | GEO
Project description:The early stages of embryonic development are critical for the proper formation of primordial germ cells. This process is tightly regulated by different cellular signals. Among others, small non-coding RNAs (sncRNAs) are involved in the regulation of these signals to carry out the embryonic development of germ cell linage. We analyzed the expression profiles of piRNAs and miRNAs after maternal exposure of embryos, during the first 13.5 days post-coitum, to two different endocrine disruptors (EDs) chemicals: vinclozolin and the main metabolite of phthalates (MEHP), in three successive generations after exposure only in the first generation. Our results indicate clear alterations in the expression of both piRNAs and miRNAs (including mitochondrial-related), concomitant with an increase in apoptotic cells in the female early folliculogenesis during this stage of development. However, the most drastic changes occur when the effect is generated by the exposure through both paternal and maternal pathways, rather than exclusively through the maternal exposure. Based on these findings, we hypothesize the existence of an "ovarian filtering" mechanism triggered by disruptor exposure and mediated by apoptotic mechanisms regulated by sncRNAs. This system, present only in the female germ cell lineage, could render a decrease in the follicle reserve in the adult life and would function as a defense mechanism to prevent the transmission of deleterious effects to subsequent generations.
2023-07-17 | GSE236810 | GEO
Project description:According to recent reports, exposure to environmental endocrine disrupting chemicals (EDs) during pregnancy may harm multiple subsequent generations. We hypothesized that EDs must directly alter DNA methylation and/or transcription in the exposed fetal germ cells to affect the grandchild. In addition, the aberrant pattern must be retained in the germ cells of the grandchild -- withstanding global epigenome remodeling -- to affect the great-grandchild. To test this hypothesis, we extensively searched for immediate and persistent epigenetic effects in purified germ cells of the exposed fetus and those of the next generation. We treated gestating female mice with previously validated doses of vinclozolin (VZ), bisphenol A (BPA), di-(2-ethylhexyl) phthalate (DEHP), or control oil, during the time when the prospermatogonia of the exposed fetus undergo global de novo DNA methylation. Using genome-wide assays, we detected changes in transcription and DNA methylation in the exposed prospermatogonia but these did not persist into the prospermatogonia of the next generation. There was no evidence for transgenerational inheritance of these epigenetic aberrations. Our results suggest that EDs exert direct epigenetic effects in the exposed fetal germ cells, but the germline corrects against deleterious effects in the next generation. Pregnant mice were gavaged daily with endocrine distruptors (VZ at 100 mg/kg/day, DEHP at 750 mg/kg/day, BPA at 0.2 mg/kg/day or control oil) starting at 12.5 days post coitum (dpc) and the G1R germ cells were purified from the exposed fetuses at 17.5 dpc. The G2R germ cells were purified from fetuses that were sired by males that had been treated in utero in a G0 mother. G1R spermatozoa were collected from adult males that had been treated in utero at the fetal stages. G2R spermatozoa were collected from adult males who were sired by in-uteo-treated males.
2015-02-18 | E-GEOD-59539 | biostudies-arrayexpress