DNA methylation in the arcuate nucleus of heifers under two nutritional schedules
Ontology highlight
ABSTRACT:
ORGANISM(S): Bos taurus
SUBMITTER: Bruna Alves
PROVIDER: E-GEOD-77782 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:DNA methylation was assessed in genomic DNA obtained from the arcuate nucleus of heifers fed to gain body weight at high (HG, n = 4) and low (LG, n = 4) rates from 4.5 to 8.5 mo of age. A methyl-CpG binding domain-based (MBD) protein assay was performed to capture fragments of methylated DNA (methylated-enriched DNA). Input (total) and methylated-enriched DNA were labeled with two different dyes and co-hybridized to a custom-designed oligonucleotide array targeted to genes associated with nutritional inputs and the control of puberty. The ratio of the log2 (enriched/input) of the normalized intensities, were determined. Data was analyzed comparing values of HG versus LG heifers.
2016-02-11 | GSE77782 | GEO
Project description:Expression level, control and intercoordination of 66 selected heart rhythm determinant (HRD) genes were compared in atria and ventricles of 4 male and 4 female adult mice. We found that genes encoding various adrenergic receptors, ankyrins, ion channels and transporters, connexins and other components of the intercalated discs form a complex network that is chamber dependent and differs between the two sexes. In addition, most HRD genes in atria had higher expression in males than in females, while in ventricles expression levels were mostly higher in females than in males. Moreover, significant chamber-differences were observed between the sexes, with higher expression in atria than ventricles for males and higher expression in ventricles than atria for females. We have ranked the selected genes according to their prominence in controlling the HRD gene web through expression coordination with the other web genes and protecting the web though their own expression stability. Interestingly, the prominence hierarchy was substantially different between the two sexes. Taken together these findings indicate that the organizational principles of the heart rhythm transcriptome are sex-dependent, with the newly introduced prominence analysis allowing identification of genes that are pivotal for the sexual dichotomy. Four adult male (M) and 4 adult female (F) mice were decapitated, the hearts removed and atria (A) and ventricles (V) collected in separate tubes. 20 µg total RNA extracted in Trizol from each of the 16 samples was reverse transcribed in the presence of fluorescent Alexa Fluor®_647 and Alexa Fluor®_555-aha-dUTPs (Invitrogen, CA) to obtain labeled cDNAs Red and green-labeled samples of biological replicas were then co-hybridized (âmultiple yellowâ strategy) overnight at 50°C with mouse MO36k oligonucleotide arrays printed by Duke University (http://microarray.genome.duke.edu/spotted-arrays) with Operon Mouse Oligo Set, version 4.0. After washing (0.1% SDS and 1% SSC) to remove the non-hybridized cDNA, each array was scanned with GenePix 4000B scanner (MDS, Toronto, Canada) and images were primarily analyzed with GenePixPro 6.0 (Axon Instruments, CA).
2009-08-12 | E-GEOD-17324 | biostudies-arrayexpress
Project description:Trypanosoma cruzi infection is a major cause of cardiomyopathy. Gene profiling studies of hearts from infected mice have revealed prominent changes in gene expression within many functional pathways. This variety of transcriptomic changes in infected mice raises the question of whether gene expression alterations in whole hearts are due to changes in infected cardiac myocytes or other cells or even to systemic effects of the infection on the heart. We employed microarrays to examine infected cardiac myocyte cultures 48 hr post-infection. Statistical comparison of gene expression levels of 2,258 well annotated unigenes in four independent cultures of infected and uninfected myocytes detected (p < 0.05) significant > 1.5 absolute fold changes in 221 (8.8%) of the sampled genes. Major categories of affected genes included those involved in immune response, extracellular matrix and cell adhesion. While changes in extracellular matrix and cell adhesion genes were anticipated, modulation of immune response genes in the infected myocytes was surprising. These findings on infected cardiac myocytes in culture reveal that altered gene expression described in the heart in Chagas disease are the consequence of both direct infection of the myocytes and resulting from presence of other cell types in the myocardium and systemic effects of infection. Transcriptomic alteration in neonatal mouse cultured cardiomyocytes induced by the parasite T.cruzi were detected by profiling and compared using AECOM mouse 32k oligonucleotide arrays hybridized in the "multiple yellow" strategy described in Iacobas et al, Biochem Biophys Res Commun. 2006 349(1):329-38.
2010-05-15 | E-GEOD-17330 | biostudies-arrayexpress
Project description:Chronic chagasic cardiomyopathy is a leading cause of heart failure in Latin American countries. About 30% of Trypanosoma cruzi-infected individuals develop this severe symptomatic form of the disease, characterized by intense inflammatory response accompanied by fibrosis deposition in the heart. We performed a microarray analysis of a mouse model of this disease and identified >5% alterations of gene expression in the heart. Most of the upregulations were associated with immune-inflammatory responses (chemokines, adhesion molecules, cathepsins and MHC molecules) and fibrosis deposition (extracellular matrix components, lysyl oxidase and Timp1). Our results indicate potentially relevant factors involved in the pathogenesis of the disease that may provide new therapeutic targets in chronic Chagasâ disease. The heart transcriptomes of 4 age-mached Trypanosoma cruzi-infected and 4 control C57Bl/6 mice were profiled and compared using Duke Mouse 30k Oligonucleotide Arrays (Operon V3.0.1) hybridized in the "multiple yellow" strategy described in Iacobas et al, Biochem Biophys Res Commun. 2006 349(1):329-38.
2010-05-15 | E-GEOD-17363 | biostudies-arrayexpress
Project description:After myocardial infarction (MI) activation of the immune system and inflammatory mechanisms, among others, can lead to ventricular remodeling and heart failure (HF). Interaction between these systemic alterations and corresponding changes in the heart has not been extensively examined in the setting of chronic ischemia. The main purpose of this study was to investigate alterations in cardiac gene and systemic cytokine profile in mice with post-ischemic HF. Plasma was tested for IgM and IgG anti-heart reactive repertoire and inflammatory cytokines. Heart samples were assayed for gene expression. Ischemic HF significantly increased the levels of serum IgM (by 5.2 fold) and IgG (by 3.6 fold) associated with remarkable content of anti-heart specificity. Comparable increase was observed in levels of circulating pro-inflammatory cytokines, such as IL-1β (3.8x) and TNF-α (6.0x). IFN-gamma was also increased in the MI group by 3.1x. However, IL-4 and IL-10 showed no significant difference between MI and sham groups. Chemokines such as MCP-1 and IL-8 were enhanced in the plasma of infarcted mice. We identified 2079 well annotated unigenes that were significantly regulated by the post-ischemic HF. Complement activation and immune response was among the most up-regulated processes. Interestingly, 21 out of the 101 quantified unigenes involved in inflammatory response were significantly up-regulated and none were down-regulated. These data indicate that post-ischemic heart remodeling is accompanied by immune mediated mechanisms that act both systemically and locally. We compared RNA samples extracted from whole hearts of control and infarcted mice samples by analyzing hybridization to AECOM 32k mouse microarrays (http://microarray1k.aecom.yu.edu/) spotted with Operon version 3.0 70-mer oligonucleotides. The hybridization protocol, the slide type and the scanner settings were uniform throughout the entire experiment to minimize the technical noise. Control (sham) and infarcted red-labeled heart samples were hybridized against an in-house prepared green-labeled universal mouse reference.
2010-06-20 | E-GEOD-18703 | biostudies-arrayexpress
Project description:Dissemination of prostate cancer (PCa) cells to the bone marrow is an early event in the disease process. In some patients, following initial treatment, disseminated tumor cells (DTC) proliferate to form active metastases after a prolonged period of undetectable disease known as tumor dormancy. Identifying mechanisms of PCa dormancy and reactivation remain a challenge due to the lack of in vitro models. Here, we characterized in vitro PCa dormancy-reactivation by inducing three apparently dormant patient-derived xenograft (PDX) lines to proliferate through tumor cell contact with each other and with bone marrow stroma. Proliferating PCa cells demonstrated tumor cell-cell contact and integrin clustering on immunofluorescence. Global gene expression analyses on proliferating cells cultured on bone marrow stroma revealed a downregulation of TGFB2 in all of the three proliferating PCa PDX lines when compared to their non-proliferating counterparts. Furthermore, constitutive activation of myosin light chain kinase (MLCK), a downstream effector of integrin-beta1 and TGF-beta2, in non-proliferating cells resumed cell proliferation. This cell proliferation was associated with an upregulation of CDK6 and a downregulation of E2F4. Taken together, our data provide evidence to support cellular adhesion and downregulation of TGFB2 as a potential mechanism by which PCa cells escape from dormancy. Targeting TGF-beta 2-associated mechanism could provide novel opportunities to prevent lethal PCa metastasis. Custom Agilent-016162 44K whole human genome expression oligonucleotide microarrays were used to profile dormant and proliferating cells isolated from three separate LuCaP xenograft lines grown in co-culture with bone marrow stromal cells isolated from a patient with PCa bone metastases. RNA from 10 cells was amplified prior to hybridization against a common reference pool of prostate tumor cell lines.
2015-10-26 | E-GEOD-64262 | biostudies-arrayexpress
Project description:Chickens divergently selected for either high growth (HG genotype) or low growth (LG genotype) at SRA-INRA, France were used to profile abdominal adipose gene expression at 7 wk of age. The HG and LG chickens are different in various phenotypic and metabolic measurements, including growth rate, abdominal fat, plasma glycemia, insulinemia, T4, T3, triglyceride and NEFA. The HG and LG chickens are valuable as a model for biomedical and agricultural traits. Massively parallel RNA sequencing (RNA-Seq) was completed on an Illumina HiSeq 2000 System for transcription analysis of HG and LG abdominal fat. Need information on data processing, statistical analysis, and differential expression. Keywords: abdominal fat, divergently selected chickens, growth, transcriptional profiling, differentially expressed genes
2015-03-14 | GSE49121 | GEO
Project description:Background: Late gestational sleep fragmentation (LG-SF) is one of the major perturbations associated with sleep apnea and other sleep disorders during pregnancy. Objectives: To investigate the effects of late LG-SF on the epigenome of visceral white adipose tissue (VWAT) in the offspring. Methods: Time-pregnant mice were exposed to LG-SF or control sleep (LG-SC) conditions during the last 6 days of gestation. We performed large-scale DNA methylation analyses using MeDIP coupled to microarrays (MeDIP-chip) in VWAT of 24-week-old LG-SF and LG-SC offspring (n=8 mice/group). Univariate multiple-testing adjusted statistical analyses were applied to identify differentially methylated regions (DMRs) between the groups. DMRs were mapped to their corresponding genes, and tested for potential overlaps with biological pathways and gene networks. Results: We detected 2148 DMRs between LG-SF and LG-SC groups (p< 0.0001, MAT algorithm). A large proportion of the DMR-associated genes have reported functions that are altered in obesity and metabolic syndrome. Overrepresented pathways and gene networks were related to metabolic regulation and inflammatory response. Conclusions: Our findings show a major role for epigenomic regulation of pathways associated to metabolic processes and inflammatory response in VWAT. Furthermore, LG-SF-induced epigenetic alterations appear to increase the susceptibility to obesity and metabolic syndrome in the offspring. 16 mouse VWAT samples were analyzed by MeDIP coupled to microarray analysis: Offspring of mothers exposed to late-gestational sleep fragmentation (n=8, LG-SF group) and offspring of mothers mouse exposed to normal sleep conditions (n=8, LG-SC group)
2015-04-02 | E-GEOD-63208 | biostudies-arrayexpress
Project description:Agilent CpG microarray in combination with enriched methylated DNA by a MBD protein were carried out in each pool of genomic DNA from primary breast tumor and matched adjacent normal tissues. 1.Common reference vs enriched methylated DNA in tumor 2. Common reference vs enriched methylated DNA in adjacent normal 3. Then compare two data indirectly
2011-02-23 | E-GEOD-27374 | biostudies-arrayexpress
Project description:Methylated DNA binding protein 2 (MBD2) has been shown to bind specific methylated promoters and suppress transcription. Here we systematically investigate MBD2 suppression by overexpressing MBD2 in MCF-10A cells and generating genome-wide promoter methylation profiles in order to identify methylation changes likely to affect gene expression levels. MCF-10A cells were infected with MBD2 lentivirus in order to increase MBD2 expression. DNA was extracted from both infected and non-infected cells and enriched for methylated DNA through the method of methylated DNA immunoprecipitation (MeDIP). Enriched and total DNA was hybridized in different channels to 244K custom microarrays (Agilent Technologies) that contained probes covering at 100bp-spacing all transcription start sites from -800bp to 200bp (human, Ensembl v44) and all microRNAs in miRBase from 250bp before to 250bp after the microRNA. Three technical replicates were hybridized for infected and non-infected cells.
2013-06-13 | E-GEOD-47857 | biostudies-arrayexpress