Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1175852 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Introduction: In the placenta, activin A affects decidualisation and trophoblast growth and invasion. Levels increase during pregnancy to peak at parturition, while premature elevation is a hallmark of several pregnancy disorders. Here we examine the impact of elevated activin A bioactivity in the inhibin α knockout (Inha KO) mouse placenta. We also investigate whether simultaneous exposure to the endocrine disruptor, diethyl-hexyl phthalate (DEHP), which impairs normal placental function, exacerbates effects on placental morphology and gene expression in this model. Methods: Litters of Inha WT, Het and KO fetuses were collected at E15.5 from time-mated Inha heterozygous pregnant mice randomly assigned to three groups: untreated, corn oil (Vehicle) or DEHP 500 mg/kg/day, from E12.5-14.5 (n=2-17). Gross and histological placental morphology was analysed, and bulk RNA-sequencing conducted. Results: Placentae of Inha WT, Het and KO fetuses exhibited no gross differences, and no differentially expressed genes. However, sex differences included a significant increase in labyrinth area and placental size from WT males compared to WT females. DEHP exposure significantly increased fetal resorption at E15.5 but yielded little differences in placental morphology. Transcript analysis identified sex- and genotype-specific transcript alterations resulting from DEHP treatment. Eight transcripts were altered by DEHP exposure across all genotypes (Cts3, Ceacam13, Gm5155, Ssr4, Sec11c, Psg18, Psg-ps1, Taf7l). Discussion: Despite minimal morphological changes, transcriptomic differences suggest that spongiotrophoblast cells and syncytiotrophoblast giant cells are key targets of DEHP exposure, with CEA family transcripts susceptible to its effects. Additionally, DEHP exposure also modulates gene transcript responses to elevated activin A.
2025-06-12 | GSE281544 | GEO
Project description:We performed bulk RNA-Seq on testes from E13.5, E15.5 and PND 0 whole testes from Inha WT and KO mouse (lacking the inhibin a gene).
2023-08-08 | GSE236618 | GEO
Project description:We performed bulk RNA-Seq on testes from adult Inha WT and KO mice (lacking the inhibin a gene).
2023-07-16 | GSE236488 | GEO
Project description:We performed bulk RNA-Seq on male fetal germ cells isolated from E13.5 and E15.5 testes from activin A-deficient mice (Inhba KO), and from E13.5 testes from mice with greater activin A bioactivity (Inha KO). The aim of this expereiment was to determine how chronic altered activin A bioactivity altered the germline transcriptome.
2022-05-26 | GSE201520 | GEO
Project description:Gene expression by bulk RNAseq in isolated mouse Hepatic Stellate Cells (HSC) YAP ko compared to HSC YAP floxed (wt).
2022-08-26 | GSE212042 | GEO
Project description:In the present study, a pregnant mouse model exposed to di(2-ethylhexyl) phthalate (DEHP, one of the most common plasticizers) during primordial follicle formation was established. The single-cell transcriptome technology was applied to investigate the roles of melatonin in ovarian cells against DEHP exposure. .
2023-11-30 | GSE246030 | GEO
Project description:Purpose: Then goal of this study id to investigate the effects of perinatal lead (32 ppm in maternal drinking water) and DEHP (25 mg per kg of chow) exposure on liver and blood DNA methylation in both PND21 and 5-month male and female mice. Methods: Enhanced reduced-representation bisulfite sequencing (ERRBS) was used to assess DNA methylation in PND21 and 5-month old DEHP-exposed, lead-exposed and control mice. Sex-specific differential methylaton analysis by DEHP and lead exposure was conducted using MethylSig R package. Results: We observed hundreds to thousands of stably modified, sex-specific differentially methylated regions in blood and liver of DEHP-exposed and lead-exposed animals at both PND21 and 5 months.
2020-07-01 | GSE150670 | GEO
Project description:The purpose of this study is to assess the potential of TOTM to induce testicular maldevelopment in the rat. We studied the effects of TOTM on the expression of genes in pathways involved in steriodogenesis and testes development. Certain phthalate esters have previously been shown to be involved in the induction of rat testicular mal-development (TMD) through effects on the expression of genes in pathways involved in steroidogenesis and testes development. In order to assess the effects of a potential alternate plasticizer, tris(2-ethylhexyl)trimellitate (TOTM), rats were exposed daily, in utero, to TOTM in order to assess the potential of this compound to induce developmental effects on the fetal testes. Pregnant rats were exposed between gestational day 12 and 19 and fetal testes RNA was analysed using whole genome microarrays. The effects of TOTM on the expression of genes in pathways involved in steroidogenesis and testes development were examined. The effects of TOTM were also compared with di(2-ethylhexyl)phthalate (DEHP), mono(2-ethylhexyl)phthalate (MEHP), an active metabolite of DEHP, and 2-ethylhexanol (2-EH), which were used as positive and negative controls, respectively. MEHP & DEHP (500mg/kg) caused a repression of genes in TMD pathways involved in cholesterol synthesis and transport (HMGCS, HMGCR, StAR, SCARB1, FDFT1, FDPS), steroidogenesis (Cyp11a, HSD3B1, SC4MOL) and testes development (INSL3, INHA). 2-EH caused minor repression of some of the genes in the TMD pathway. This was rationalised on the basis that 2-EH, a DEHP metabolite, is also a weak PPARα agonist. It has been shown that in utero treatment with DBP will repress the genes from fetal testes involved in steroidogenesis and that this effect is associated with direct DBP-mediated binding of PPARα to the promoters of these genes (Plummer et. al. 2010). TOTM did not cause a significant repression of genes in the TMD pathway. Based on these data, it is highly unlikely that TOTM will cause testicular dysgenesis in rats. Rats were exposed to TOTM in utero by the administration of daily oral gavage doses to pregnant dams between gestational day 12 and 19. The foetal testes were obtained by micro-dissection and prepared to facilitate the isolation of RNA, which was subsequently analysed using whole rat genome microarrays.
2012-10-30 | E-GEOD-41901 | biostudies-arrayexpress
Project description:BACKGROUND: Phthalates are manmade industrial additives used mostly as plasticizers. In addition to their deleterious effects on male genital development, population studies have recently documented correlations between phthalates exposure and subtle impacts on reproductive tract development and on the metabolic syndrome in male adults. In mature rodents liver di-(2-ethylhexyl)-phthalate (DEHP) activates the peroxisome proliferators-activated receptor (PPARalpha), a member of the nuclear receptor (NR) superfamily. OBJECTIVES: Using a systems biology approach, we aimed at defining potential mechanisms underlying the impacts of DEHP on adult mouse liver and testis. METHODS: Thus, we performed a parallel analysis of transcript and metabolic profiles in the liver from adult mice exposed to varying DEHP doses. Moreover, we obtained pangenomic mRNA profiles of laser-captured Leydig and Sertoli cells from mature animals exposed to DEHP. RESULTS: Hepatic genes modulated by DEHP are predominantly PPARalpha targets. However, the induction of some prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways. Integration of hepatic transcriptomic and metabonomic profiles further revealed a correlation between the impacts of DEHP on a cluster of genes and metabolites linked to heme synthesis and on a cluster of Rev-erbalpha target genes related to metabolic and circadian clock pathways. Cell-specific effects of DEHP were investigated in the adult testis and a noticeable impact of DEHP was observed on Leydig cells transcriptome. CONCLUSIONS: We report a detailed analysis of DEHP interference with hepatic Constitutive Androstane Receptor (CAR) and Rev-erbalpha pathways and a novel transcriptional impact of DEHP on adult endocrine cells of the testis. Keywords: Treatment effect
2009-02-19 | GSE13240 | GEO
Project description:BACKGROUND: Phthalates are manmade industrial additives used mostly as plasticizers. In addition to their deleterious effects on male genital development, population studies have recently documented correlations between phthalates exposure and subtle impacts on reproductive tract development and on the metabolic syndrome in male adults. In mature rodents liver di-(2-ethylhexyl)-phthalate (DEHP) activates the peroxisome proliferators-activated receptor (PPARalpha), a member of the nuclear receptor (NR) superfamily. OBJECTIVES: Using a systems biology approach, we aimed at defining potential mechanisms underlying the impacts of DEHP on adult mouse liver and testis. METHODS: Thus, we performed a parallel analysis of transcript and metabolic profiles in the liver from adult mice exposed to varying DEHP doses. Moreover, we obtained pangenomic mRNA profiles of laser-captured Leydig and Sertoli cells from mature animals exposed to DEHP. RESULTS: Hepatic genes modulated by DEHP are predominantly PPARalpha targets. However, the induction of some prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways. Integration of hepatic transcriptomic and metabonomic profiles further revealed a correlation between the impacts of DEHP on a cluster of genes and metabolites linked to heme synthesis and on a cluster of Rev-erbalpha target genes related to metabolic and circadian clock pathways. Cell-specific effects of DEHP were investigated in the adult testis and a noticeable impact of DEHP was observed on Leydig cells transcriptome. CONCLUSIONS: We report a detailed analysis of DEHP interference with hepatic Constitutive Androstane Receptor (CAR) and Rev-erbalpha pathways and a novel transcriptional impact of DEHP on adult endocrine cells of the testis. Keywords: Treatment effect
2009-02-19 | GSE13237 | GEO