Estrogen inhibits lipid content in liver exclusively from membrane receptor signaling
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Harry Harvey
PROVIDER: E-GEOD-45346 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Membrane estrogen receptor (ER) alpha stimulates AMP kinase to suppress SREBP1 processing and lipids in liver Here we present evidence that signaling from membrane-localized ERalpha similarly suppresses a subset of mRNAs in the livers of female WT and membrane only estrogen receptor (MOER) transgenic mice but not in estrogen receptor knock out (ERKO) mice
2013-05-14 | GSE45346 | GEO
Project description:We investigated gene expression levels in Heliconius erato butterflies with divergent wing patterns across a 656KB genomic interval linked to the red color pattern wing polymorphism. This included comparison of expression between two H. erato color pattern populations (H. e. petiverana and a H.e. etylus x H. himera hybrid) across three sections of the forewing that differed in pigmentation (the basal, mid, and distal wing sections) and five different stages of pupal development (Day 1, 3, 5 pupae and ommochrome and melanin pigmentation stages). These results allowed us to determine whether certain genes in this interval were differentially expressed between the wing pattern elements, and, therefore, potentially responsible for adaptive color pattern variation in these butterflies. Forewings from a total of 29 individuals, covering three biological replicates of five developmental time points for each of the two H. erato distinct phenotypes were dissected, with the only exception being that there were only two replicates of the day 1 hybrid phenotype. Individuals were reared at 25˚C and dissected at the following stages: a) day 1 = 12 hr after pupation; b) day 3 = 60 hr after pupation; c) day 5 = 108 hr after pupation; d) early ommochrome = ~ 156 hr after pupation when red scales in forewing partially mature, showing a pale orange color; and e) early melanin = ~ 180 hr after pupation melanic scales begin to turn black and are present primarily at the center of the wing. Using wing veins as landmarks, each forewing was cut into three sections corresponding to the color pattern boundaries: basal (F1), middle (F2), and apical (F3). A eight custom-designed Roche NimbleGen 12x135K format microarrays with probes spanning a 656,307bp genomic region (Roche NimbleGen Inc., Madison, Wisconsin, United States) were used to hybridize double stranded cDNA from 87 tissue samples. Repetitive sequence elements found more than five times across all currently available H. erato genomic sequences, including the probed region as well as additional genomic BAC sequences, were masked from the tiling region. The remaining unmasked non-repetitive genomic sequences were tiled using 60 bp probes staggered every 13 bp on average, with slight modifications to ensure probe quality, for a total of 48,547 probes. Microarry design and printing was performed by Roche NimbleGen. cDNA labeling, hybridization, and array scanning was performed by the City of Hope Microarray Facility (Duarte, California, United States). In addition to the probes from the red color pattern intervals, the arrays also include 40,763 probes across two other genomic intervals not addressed in this study, 45,046 probes representing 12450 transcripts from a recent transcriptome assembly at 1-6X coverage, and 3248 random probes. Results from the transcriptome and other color pattern intervals will be published separately, however, we analyzed all probes together for array normalization and quality control.
2011-12-02 | E-GEOD-30221 | biostudies-arrayexpress
Project description:Estrogen receptor alpha (ERa) is required for the protective effects of 17-beta-estradiol (E2, the active, endogenous form of estrogen) after vascular injury or in atherosclerosis. E2-bound ERa can function as a transcription factor which binds directly to chromatin (the genomic pathway). Some ERa is also associated with the plasma membrane and, when bound by E2, activates cellular kinases, including PI3K, Akt and ERK (the rapid signaling pathway). Rapid signaling is mediated by interaction between ERa and the adaptor molecule striatin. Here we identify a triple point mutation (AA 231,233 & 234 KRR->AAA) of full length ERa that blocks its association with striatin and eliminates its ability to perform rapid signaling (without affecting its ability to perform genomic signaling). We have created stably-transfected human vascular endothelial cell lines expressing either WT ERa (WT ECs) or KRR mutant ERa (KRR ECs), and use these cells to show that rapid signaling through ERa is required for the proper regulation of most E2-regulated genes (the data presented in this record), and also for the ability of E2 to stimulate EC migration and proliferation and to inhibit inflammatory monocyte adhesion to ECs. Human Eahy 926 stable cell lines carrying a full length wild-type human estrogen receptor alpha (ERa) expression vector (WT ECs) or a full length KRR mutant ERa expression vector (KRR ECs, where the KRR mutant ERa is deficient in rapid signaling) were treated with or without 17-b-estradiol (E2) for 16 hrs. RNA from 3 bioligical replicates per condition was harvested and used to probe Illumina bead arrays.
2016-03-22 | E-GEOD-72180 | biostudies-arrayexpress
Project description:Gene expression profiling was performed on CNS tissue from neonatal mice carrying the T9H translocation and maternal or paternal duplication of proximal Chromosomes 7 and 15. Our analysis revealed the presence of two novel paternally expressed intergenic transcripts at the PWS/AS locus. The transcripts were termed Pec2 and Pec3 for paternally expressed in the CNS.Our analysis also revealed imprinting of Magel2, Mkrn3, Ndn,Ube3a and Usp29, as well as Pec2 and Pec3 in embryonic brain, 15.5 dpc, and provided a survery of biallelically expressed genes on proximal Chromosomes 7 and 15 in embryonic and neonatal CNS. Experiment Overall Design: Eight samples were analyzed by microarray analysis using GeneChip 430B (no biological replicates). RNAs were from neonatal cortex and cerebellum, and from whole brain of 13.5 and 15.5 dpc embryos, purified from mice carrying either maternal or paternal duplication of proximal chromosomes 7 and 15.
2008-10-21 | E-GEOD-12230 | biostudies-arrayexpress
Project description:Gene expression profiling was performed on CNS tissue from neonatal mice carrying the T9H translocation and maternal or paternal duplication of proximal Chromosomes 7 and 15. Our analysis revealed the presence of two novel paternally expressed intergenic transcripts at the PWS/AS locus. The transcripts were termed Pec2 and Pec3 for paternally expressed in the CNS.Our analysis also revealed imprinting of Magel2, Mkrn3, Ndn,Ube3a and Usp29, as well as Pec2 and Pec3 in embryonic brain, 15.5 dpc, and provided a survery of biallelically expressed genes on proximal Chromosomes 7 and 15 in embryonic and neonatal CNS. This SuperSeries is composed of the following subset Series:; GSE12227: Neonatal and embyronic CNS of mice with maternal or paternal duplication of proximal chromosomes 7 and 15 (430A); GSE12230: Neonatal and embyronic CNS of mice with maternal or paternal duplication of proximal chromosomes 7 and 15 (430B) Experiment Overall Design: Refer to individual Series
2008-10-21 | E-GEOD-12231 | biostudies-arrayexpress
Project description:Estrogen-based treatments have numerous extra-reproductive effects. On the one hand, they have protective metabolic actions against abdominal fat accumulation, type 2 diabetes, liver steatosis,⦠But, on the other hand, the oral route of administration, presumably due to a hepatic impact on liver-derived coagulation factors, appears to increase risks of venous thrombosis and pulmonary embolism. The characterization of liver genes expression regulations by these hormones thereby appears of utmost interest, but the estrogen-sensitive transcriptome of liver and ER cistrome was so far explored under chronic hormonal treatment. To explore the early steps of these mechanisms, we determined here the short-term changes in liver transcriptional responses to acute E2 administration, and aimed to characterize the mechanisms allowing these programs to be engaged. Collectively, through the comparison of mice expressing or not ER, our data demonstrate that acute administration of E2 provokes genes expression variations which fit with a crucial role of ER in the prevention of liver steatosis in mice fed with a high fat diet by E2. They also evidenced higher proportion of ER binding sites (BSs) located at the direct vicinity (distance <3kb) of regulated genes than what is determined in human cancer cell models. Besides this specific aspect of ER cistrome in vivo, we unexpectedly found that 40 % of the BSs of the pioneer factor Foxa2 were dependent upon the expression of ER that indirectly influences the distribution of the nucleosomes harbouring a dimethylated H3K4 around these Foxa2 sites. Analysis of estrogen-sensitive and estrogen receptor (ER)-dependent transcriptomes in livers from wild-type or ERKO mice.
2016-05-13 | E-GEOD-70329 | biostudies-arrayexpress
Project description:Small non-coding RNA biogenesis typically involves cleavage of structured precursors by RNase III-like endonucleases. However, guide RNAs that direct U-insertion/deletion mRNA editing in mitochondria of trypanosomes maintain 5â² triphosphate characteristic of transcription start site and possess U-tail indicative of 3â² processing and uridylation. Here, we identified a protein complex composed of RET1 TUTase and 3â²-5â² DSS1 exonuclease, and three additional subunits. This complex, termed mitochondrial 3â² processome (MPsome), is responsible for primary uridylation of ~800-nt gRNA precursors, their processive degradation to a mature length of 50-60 nt, and secondary U-tail addition. Both strands of gRNA gene are transcribed giving rise to sense and antisense precursors of similar size. Head-to-head hybridization of these transcripts blocks symmetrical 3â²-5â² degradation at the fixed distance from the double-stranded region. Together, our findings suggest a model in which gRNA is derived from the 5â² extremity of a primary molecule by uridylation-induced, antisense transcription-controlled exonucleolytic degradation. 1. we first sequenced guide RNA precursor (Gel-fractioned total cellular RNA 600-1500nt was used) transcripts from three replicates to study the their tail features and also validate observation of sense/antisense accumulation upon perturbation of pre-processing complex based on few cases. 2. we then sequenced mitochondrial small RNA and built a reference for small RNAs using our custom algorithm. We then took the mitochondrial small RNA data and uncovered the sense/antisense pair. 3. We then used CLIP-Seq data to investigate in vivo binding sites and, together with RNA IP-Seq data to understand what determine the relative abundance of sense and antisense pair of the duplex. 4. We used sequenced small mitochondrial RNA in different RNAi experiments (For RNAi experiments, 30-70nt RNA fraction was gel-isolated from total cellular RNAs) to understand which protein will affect the Utail length in mature small mitochondrial RNA.
2016-02-08 | E-GEOD-71292 | biostudies-arrayexpress
Project description:Evaluation of Estrogen receptor related gene expression in C57BL/6 vs ERKO-alpha and ERKO-beta mice
| PRJNA120119 | ENA
Project description:Two subtypes of the estrogen receptor, ERalpha and ERbeta, mediate the actions of estrogens, and the majority of human breast tumors contain both ERalpha and ERbeta. To examine the possible interactions and modulatory effects of ERbeta on ERalpha activity, we have used adenoviral gene delivery to produce human breast cancer (MCF-7) cells expressing ERbeta, along with their endogenous ERalpha. We have examined the effects of ERβ expression on genome-wide gene expression by Affymetrix GeneChip microarrays. We find that ERbeta modulated estrogen gene expression on nearly 24% of E2-stimulated genes but only 8% of E2-inhibited genes. We find that ERbeta modulation is gene-specific, enhancing or counteracting ERalpha regulation for distinct subsets of estrogen target genes. Introduction of ERbeta into ERalpha-containing cells induced up/down-regulation of many estrogen target in the absence of any added ligand. In addition, ERbeta presence elicited the expression of a unique set of genes that were not regulated by ERalpha alone. ERbeta modulated the expression of genes in many functional categories, but the greatest numbers were associated with transcription factor and signal transduction pathways. Regulation of multiple components in the TGF beta, SDF1, and semaphorin pathways, may contribute to the suppression of proliferation observed with ERbeta both in the presence and absence of estrogen. Hence, ERbeta modulates ERalpha gene regulation in diverse ways that may contribute to its growth-inhibiting beneficial effects in breast cancer Experiment Overall Design: MCF-7 cells expressing endogenous ERalpha were infected with adenovirus carrying either estrogen receptor beta (AdERb) or no insert (Ad) at multiplicity of infection (moi) of 5 or 50. Cells were infected with adenovirus for a period of 48hr before treatment with ligand (vehicle control or 10nM 17beta-estradiol) for a additional period of 24hr before harvest.
2009-04-24 | E-GEOD-4006 | biostudies-arrayexpress
Project description:Estrogen receptor beta (ERβ) is a ligand inducible transcription factor regulating gene expression in response to the female sex hormone estrogen. Previously, we found that ERβ deficiency results in changes in DNA methylation patterns at two gene promoters, implicating an involvement of ERβ in DNA methylation. In this study, we set out to explore this involvement on a genome-wide level, and to investigate the underlying mechanisms of this function. Using reduced representation bisulfite sequencing (RRBS), we compared genome-wide DNA methylation in mouse embryonic fibroblasts (MEFs) derived from wildtype (wt) and ERβ knock-out (βerko) mice, and identified around 8000 differentially methylated positions (DMPs). This suggests that ERβ is involved in regulating DNA methylation at specific sites in the genome. Genome-wide DNA methylation was analysed in MEFs derived from wildtype and ERbeta null mice by educed representation bisulfite sequencing (RRBS) on an Illumina Genome Analyser IIx platform.
2016-02-22 | E-GEOD-72230 | biostudies-arrayexpress