Ontology highlight
ABSTRACT:
PROVIDER: PRJNA661686 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12599100_1.fastq.gz | Fastqsanger.gz | |||
| SRR12599100_2.fastq.gz | Fastqsanger.gz | |||
| SRR12599101_1.fastq.gz | Fastqsanger.gz | |||
| SRR12599101_2.fastq.gz | Fastqsanger.gz | |||
| SRR12599102_1.fastq.gz | Fastqsanger.gz |
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Project description:17β-estradiol (E2) is an important endocrine hormone underlying mammalian body, which participates in the regulatory of physiological functions of reproductive system, mammary gland, bone and cardiovascular, et.al. Paradoxically, despite the physiological actions of endogenous E2 (0.2-1.0 nmol/L), numerous clinical and experimental studies demonstrated that high-dose E2 treatment could cause tumor regression and exert pro-apoptotic actions in multiple cells, but the underlying mechanism is still undescribed. Especially, little information of cellular processes responding to lethality of 17β-estradiol is available. In the present work, we attempted to characterize the cellular processes responding to high-dose (mol/L) E2 treatment by quantitative phosphoproteomics to help understand the regulatory mechanism of E2 induced cell death. Therefore, to analyze the cell phenotype induced by high-dose (umol/L) E2, cell counting kit-8 assay (CCK8), cell cytotoxicity analysis by trypan blue staining and microscopy imaging were first performed on HeLa cells following 1-10 mol/L E2 or dimethyl sulfoxide (DMSO) treatment for 1-3 days. As a result, E2 was found to inhibit cell proliferation and induce cell death in a dose-dependent and time-dependent fashion. Specially, in comparison with DMSO-treated HeLa cell samples, 5 umol/L E2 treatment for 2 days resulted in > 74% of growth inhibition and about 50% of cell death, which was employed for following quantitative phosphoproteomic analysis. To investigate the intracellular cellular processes responding to high-dose (umol/L) E2 treatment, solid phase extraction (SPE)-based immobilized titanium ion affinity chromatography (Ti-IMAC) phosphopeptide enrichment method coupled with data independent acquisition (DIA)-based quantitative proteomics was employed for in-depth screening of high-dose E2 regulated phosphorylation sites. As a result, more than 10000 phosphorylation sites were identified from the E2 and DMSO treated HeLa cell samples by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Among these phosphorylation sites, in comparison with the DMSO-treated cell samples, 5 umol/L E2 treatment caused an increase of 537 phosphorylation sites on 372 proteins and a decrease of 387 phosphorylation sites on 256 proteins with a threshold of p-value < 0.01 and |fold change|≥2. Totally 924 phosphorylation sites on 599 proteins were significantly regulated by high-dose (umol/L) E2, which were then performed for enrichment analysis. In addition, 453 phosphorylation sites on 325 proteins were found to be identified in only E2 or DMSO treated cell samples. These phosphorylation sites probably be phosphorylated or de-phosphoylated responding to high-dose E2 stimulation, which likely be regulated by high-dose (umol/L) E2 and were also performed for enrichment analysis in parallel. Taken together, 1218 phosphorylation sites on 741 proteins were significantly regulated by high-dose E2.
2024-07-05 | PXD043554 | JPOST Repository
Project description:Early life exposure to antibiotics alters the gut microbiome. These alterations lead to changes in metabolic homeostasis and an increase in host adiposity. We used microarrays to identify metabolic genes that may be up- or down-regulated secondary to antibiotic exposure. Low dose antibiotics have been widely used as growth promoters in the agricultural industry since the 1950’s, yet the mechanisms for this effect are unclear. Because antimicrobial agents of different classes and varying activity are effective across several vertebrate species, we hypothesized that such subtherapeutic administration alters the population structure of the gut microbiome as well as its metabolic capabilities. We generated a model of adiposity by giving subtherapeutic antibiotic therapy (STAT) to young mice and evaluated changes in the composition and capabilities of the gut microbiome. STAT administration increased adiposity in young mice and altered hormones related to metabolism. We observed substantial taxonomic changes in the microbiome, changes in copies of key genes involved in the metabolism of carbohydrates to short-chain fatty acids (SCFA), increases in colonic SCFA levels, and alterations in the regulation of hepatic metabolism of lipids and cholesterol. In this model, we demonstrate the alteration of early life murine metabolic homeostasis through antibiotic manipulation. C57BL6 mice were divided into low-dose penicillin or control groups. Given antibiotics via drinking water after weaning. Sacrificed and liver sections collected for RNA extraction.
2012-06-30 | E-GEOD-38880 | biostudies-arrayexpress
Project description:Clinical treatment protocols for infertility with in vitro fertilization-embryo transfer (IVF-ET) provide a unique opportunity to assess the human vaginal microbiome in defined hormonal milieu. Herein, we have investigated the association of circulating ovarian-derived estradiol (E2) and progesterone (P4) concentrations to the vaginal microbiome. Thirty IVF-ET patients were enrolled in this study, after informed consent. Blood was drawn at four time points during the IVF-ET procedure. In addition, if a pregnancy resulted, blood was drawn at 4-to-6 weeks of gestation. The serum concentrations of E2 and P4 were measured. Vaginal swabs were obtained in different hormonal milieu. Two independent genome-based technologies (and the second assayed in two different ways) were employed to identify the vaginal microbes. The vaginal microbiome underwent a transition with a decrease in E2 (and/or a decrease in P4). Novel bacteria were found in the vagina of 33% of the women undergoing IVF-ET. Our approach has enabled the discovery of novel, previously unidentified bacterial species in the human vagina in different hormonal milieu. While the relationship of hormone concentration and vaginal microbes was found to be complex, the data support a shift in the microbiome of the human vagina during IVF-ET therapy using standard protocols. The data also set the foundation for further studies examining correlations between IVF-ET outcome and the vaginal microbiome within a larger study population.
2011-10-24 | E-MEXP-2958 | biostudies-arrayexpress
Project description:Time and dose related expression profiles of rat right heart tissue in microsphere bead model for Pulmonary embolism Experiment Overall Design: Rat right tissues of the Vehicle(no beads- control), low dose and high dose from rat bead model for Pulmonary Embolism were collected after 2, 6 and 18 hour time points. The extracted RNA was hybridized to Affymetrix Rat 230-2.0 microarrays to look for the dose and/or time related transcriptional changes associated with experimental Pulmonary Embolism.
2008-10-18 | E-GEOD-6104 | biostudies-arrayexpress
Project description:Proteomics of High dose of TCM，model and normal in rat
2024-03-03 | PXD050293 |
Project description:Time and dose related expression profiles of rat right heart tissue in microsphere bead model for Pulmonary embolism Keywords: Time course and dose response in experimental PE
2008-07-01 | GSE6104 | GEO
Project description:Bisphenol A (BPA) is primarily used to make polycarbonate plastic, with a global capacity of production exceeding 8 million tons per year. Biomonitoring studies with human urine, blood and tissue samples suggest that humans are subjected to widespread and continuous exposure to BPA. It has been well established that early life exposure to BPA predisposes the prostate gland to carcinogenesis later in life. However, it remains unknown if BPA exposure during adulthood induces benign or neoplastic pathology in the prostate. The main objective of the present study is to determine the effects of BPA exposures during adulthood on the prostate and to characterize the global transcriptional reprogramming underlying endocrine disruption by BPA. We elevated circulating levels of free BPA in Noble rats to the human-relevant internal dose range with BPA-filled Silastic implants while maintaining the physiological levels of testosterone (T) with T-filled implants. Cotreatment with T and 17β-estradiol (E2) was our reference regimen which induced preneoplastic and cancereous lesions. The T + low/high dose of BPA induced prostatic hyperplasia, low-grade prostate intraepithelial neoplasia (LGPIN) and intraepithelial infiltration of T-lymphocytes specifically in the lateral prostate (LP). Using microarray analysis, we delineated specific impacts of low and high dose of BPA (with the T-support) on the gene expression program in LPs. Hierarchical clustering revealed that the endocrine disrupting effects of T + low dose of BPA showed partial resemblance to those of T + high dose of BPA and T+E2. In contrast, the influence of T+ high dose of BPA on the LP transcriptome was completely different from those of T + E2. Further, IPA analysis of specific T+ low or high BPA gene signature identified a transcription factor, HNF4α, as a regulatory hub affecting a number of differentially expressed genes by BPA exposures. These findings suggest that the adult rat prostate is still venerable to the endocrine disrupting effects of BPA. Perhaps chronic exposure to low dose of BPA provides a niche comprising heightened cell proliferation, inflammatory responses and disrupted gene expression program, which favor the onset and development of prostatic benign or malignant diseases in men. Rat lateral prostates were collected from untreated control and treated groups [Testosterone (T) + Estradiol (E2), T + low dose Bisphenol A (low BPA) and T + high BPA] for RNA extraction and hybridization on Affymetrix microarrays. We sought to identify transcriptional signature of BPA exposures in the lateral prostate gland.
2015-03-07 | E-GEOD-66633 | biostudies-arrayexpress
Project description:To obtain comprehensive information on 17beta-estradiol (E2) sensitivity of genes that are inducible or suppressible by this hormone, we designed a method that determines ligand sensitivities of large numbers of genes using DNA microarray and a set of simple Perl computer scripts implementing the standard metric statistics, and employed it to characterize effects of low (0-100 pM) concentrations of E2 on the transcriptome profile of MCF7/BUS human breast cancer cells, whose E2 dose-dependent growth curve saturated with 100 pM E2. Evaluation of changes in mRNA expression for all genes covered by the DNA microarray indicated that, at a very low concentration (10 pM), E2 suppressed 3~5 times larger numbers of genes than it induced, whereas at higher concentrations (30-100 pM) it induced 1.5~2 times more genes than it suppressed. Using clearly defined statistical criteria, E2-inducible genes were categorized into several classes based on their E2 sensitivities. This approach of hormone sensitivity analysis revealed that expression of two previously reported E2-inducible autocrine growth factors, TGF-? and SDF-1, was not affected by 100 pM and lower concentrations of E2 but strongly enhanced by 10 nM E2, which was far higher than the concentration that saturated the E2 dose-dependent growth curve of MCF7/BUS cells. These observations suggested that biological actions of E2 are derived from expression of multiple genes whose E2 sensitivities differ significantly and, hence, dependent on the E2 concentration especially when it is lower than the saturating level, emphasizing the importance of characterizing the ligand dose-dependent aspects of E2 actions. (paper abstract) Keywords: Dose Response, Time Course
2006-04-14 | GSE4668 | GEO