Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nanostring gene expression analysis of splenocytes from 17-β estradiol (E2) and synthetic 17α-ethinyl estradiol (EE) exposed feamle NZB/WF1 lupus mice

ABSTRACT: We used the NanoString mouse nCounter immunology panel platform to compare mRNA gene expression profiles of spelnocytes from placebo-, E2, and EE exposed NZB/WF1 mice. With the profling of 548 immunology-related genes, we found that E2 and EE exposure alter immune-related genes at a similar pattern.

ORGANISM(S): Mus musculus Mus musculus domesticus

PROVIDER: GSE121743 | GEO | 2018/12/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Nanostring miRNA exprssion profiling analysis of splenocytes from 17-β estradiol (E2) and synthetic 17α-ethinyl estradiol (EE) exposed feamle NZB/WF1 lupus mice

Project description:We used the NanoString mouse nCounter miRNA expression platform to compare the miRNA expression profiles of spelnocytes from placebo-, E2, and EE exposed NZB/WF1 mice. We found that EE exposure has a more profound effect than E2 on miRNA genes expression in splenocytes

2018-12-10 | GSE121744 | GEO

Nanostring expression analysis of splenocytes from 17-β estradiol (E2) and synthetic 17α-ethinyl estradiol (EE) exposed feamle NZB/WF1 lupus mice

Project description:Nanostring expression analysis of splenocytes from 17-β estradiol (E2) and synthetic 17α-ethinyl estradiol (EE) exposed feamle NZB/WF1 lupus mice

| PRJNA498302 | ENA

Nanostring gene expression analysis of splenocytes from 17-β estradiol (E2) and synthetic 17α-ethinyl estradiol (EE) exposed feamle NZB/WF1 lupus mice

Project description:Nanostring gene expression analysis of splenocytes from 17-β estradiol (E2) and synthetic 17α-ethinyl estradiol (EE) exposed feamle NZB/WF1 lupus mice

| PRJNA498303 | ENA

Nanostring miRNA exprssion profiling analysis of splenocytes from 17-β estradiol (E2) and synthetic 17α-ethinyl estradiol (EE) exposed feamle NZB/WF1 lupus mice

Project description:Nanostring miRNA exprssion profiling analysis of splenocytes from 17-β estradiol (E2) and synthetic 17α-ethinyl estradiol (EE) exposed feamle NZB/WF1 lupus mice

| PRJNA498304 | ENA

17β-Estradiol and 17α-Ethinyl Estradiol Exhibit Immunologic and Epigenetic Regulatory Effects in NZB/WF1 Female Mice.

Project description:17α-Ethinyl estradiol (EE), a synthetic analog of natural estrogen 17β-estradiol (E2), is extensively used in hormonal contraceptives and estrogen replacement therapy, and it has also been found in sewage effluents. Given that E2 is a well-known immunomodulator, surprisingly there has been only limited information on the cellular and molecular immunologic consequences of exposure to EE. To address this fundamental gap, we directly compared the effects of EE with E2 on splenic leukocytes of New Zealand Black × New Zealand White F1 progeny (NZB/WF1) mice during the preautoimmune period. We found that EE and E2 have common, as well as distinctive, immunologic effects, with EE exposure resulting in more profound effects. Both EE and E2 increased numbers of splenic neutrophils, enhanced neutrophil serine proteases and myeloperoxidase expression, promoted the production of nitric oxide and monocyte chemoattractant protein-1, and altered adaptive immune T cell subsets. However, activation of splenic leukocytes through the T cell receptor or Toll-like receptor (TLR)4 revealed not only common (IL-10), but also hormone-specific alterations of cytokines (IFNγ, IL-1β, ΤΝFα, IL-2). Furthermore, in EE-exposed mice, TLR9 stimulation suppressed IFNα, in contrast to increased IFNα from E2-exposed mice. EE and E2 regulated common and hormone-specific expression of immune-related genes. Furthermore, EE exposure resulted in more marked alterations in miRNA expression levels than for E2. Only EE was able to reduce global DNA methylation significantly in splenic leukocytes. Taken together, our novel data revealed that EE and E2 exposure confers more similar effects in innate immune system-related cell development and responses, but has more differential regulatory effects in adaptive immune-related cell development and responses.

| S-EPMC6305969 | biostudies-literature

Nanostring expression analysis of splenocytes from 17-β estradiol (E2) and synthetic 17α-ethinyl estradiol (EE) exposed feamle NZB/WF1 lupus mice

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

2018-12-10 | GSE121745 | GEO

Characterizing transcriptional responses of the Ishikawa cell line to ethinyl estradiol (EE; CAS #57-63-6) following 72 hour exposure

Project description:A toxicity pathway approach was taken to develop an in vitro assay using human uterine epithelial adenocarcinoma (Ishikawa) cells (ECACC cat#99040201) as a replacement for measuring an in vivo uterotrophic response to estrogens. As part of validating the use of this cell line, gene arrays were performed to confirm functional transcriptional responses to ethinyl estradiol (EE)

2017-07-01 | GSE84711 | GEO

Estrogen-like disruptive effects of dietary exposure to bisphenol A or 17α-ethinyl estradiol in CD1 mice.

Project description:Bisphenol A (BPA) is an endocrine disrupting chemical that is ubiquitous in wild and built environments. Due to variability in study design, the disruptive effects of BPA have proven difficult to experimentally replicate. This study was designed to assess the disruptive actions of dietary BPA exposure, while carefully controlling for known confounders. Parental CD1 mice were acclimated to defined diet containing BPA (0.03, 0.3, 3, 30, or 300 ppm) or 17α-ethinyl estradiol (EE; 0.0001, 0.001, and 0.01 ppm) and bred to produce progeny (F1) that were maintained through adulthood on the same diet as the parents. In F1 females, uterine weights were increased in all EE and the 30-ppm BPA-exposure groups, demonstrating model sensitivity and estrogen-like actions of BPA. In BPA-exposed females, no treatment-related differences were observed in parental reproductive function, or in the timing of puberty and metabolic function in female offspring. In F1 males, modest changes in body weight, adiposity and glucose tolerance, consistent with improved metabolic function, were observed. Associated with increased prolactin and increased circulating testosterone levels, balanopreputial separation was accelerated by 0.03 and 3.0 ppm BPA and anogenital distance at postnatal day 21 was increased in males by 0.03 ppm BPA. Sperm counts were also increased with 3.0 ppm BPA exposures. Overall, BPA was found to have modest, sex specific endocrine disruptive effects on a variety of end points below the established no observed adverse effect level. The dose response characteristics for many of the effects were nonmonotonic and not predictable from high-dose extrapolations.

| S-EPMC5384470 | biostudies-literature

Low-dose 17?-ethinyl estradiol (EE) exposure exacerbates lupus renal disease and modulates immune responses to TLR7/9 agonists in genetically autoimmune-prone mice.

Project description:Estrogens have been shown to regulate the immune system and modulate multiple autoimmune diseases. 17?-ethinyl estradiol (EE), a synthetic analog of 17?-estradiol, is prescribed commonly and found in oral contraceptives and hormone replacement therapies. Surprisingly, few studies have investigated the immunoregulatory effects of exposure to EE, especially in autoimmunity. In this study, we exposed autoimmune-prone female MRL/lpr mice to a human-relevant dose of EE through the oral route of exposure. Since lupus patients are prone to infections, groups of mice were injected with viral (Imiquimod, a TLR7 agonist) or bacterial (ODN 2395, a TLR9 agonist) surrogates. We then evaluated autoimmune disease parameters, kidney disease, and response to in vivo TLR7/9 pathogenic signals. EE-exposed mice had increased proteinuria as early as 7 weeks of age. Proteinuria, blood urea nitrogen, and glomerular immune complex deposition were also exacerbated when compared to controls. Production of cytokines by splenic leukocytes were altered in EE-exposed mice. Our study shows that oral exposure to EE, even at a very low dose, can exacerbate azotemia, increase clinical markers of renal disease, enhance glomerular immune complex deposition, and modulate TLR7/9 cytokine production in female MRL/lpr mice. This study may have implications for EE-exposure risk for genetically lupus-prone individuals.

| S-EPMC7090002 | biostudies-literature

Strain specific induction of pyometra and differences in immune responsiveness in mice exposed to 17α-ethinyl estradiol or the endocrine disrupting chemical bisphenol A.

Project description:Pyometra is an inflammatory disease of the uterus that can be caused by chronic exposure to estrogens. It is unknown whether weakly estrogenic endocrine disruptors can cause pyometra. We investigated whether dietary exposures to the estrogenic endocrine disruptor bisphenol A (BPA) induced pyometra. Pyometra did not occur in CD1 mice exposed to different dietary doses of BPA ranging from 4.1 to >4000μg/kg-d or 17α-ethinyl estradiol (EE; 1.2 to >150μg/kg-d). In the C57BL/6 strain, pyometra occurred in the 15μg/kg-d EE and 33μg/kg-d BPA treatment groups. At the effective concentration of BPA, histological analysis revealed pathological alterations of uterine morphology associated with a >5.3-fold increase in macrophage numbers in non-pyometra uteri of C57BL/6 mice exposed to BPA. These results suggest that BPA enhances immune responsiveness of the uterus and that heightened responsiveness in C57BL/6 females is related to increased susceptibility to pyometra.

| S-EPMC3367079 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data