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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse primary dermal fibroblasts treated with DNA demethylating agent 5-aza-2-deoxycytidine

ABSTRACT: Mouse primary dermal fibroblasts were treated with DNA demethylating agent 5-aza-2'-deoxycytidine. The exposure was 5um 5A2dC for 96 hours followed by recovery in normal medium for 24 hours. Three biological replicates were created for both the control and treated populations. Each biological replicate represents a separate derivation of dermal fibroblasts from genetically identical mouse pups aged 0-3 days. Cells reached passage 4 before initiating drug exposure.

ORGANISM(S): Mus musculus

SUBMITTER: Tammy Vallender

PROVIDER: E-MEXP-701 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Localized methylation in the key regulator gene endothelin-1 is associated with cell type-specific transcriptional silencing.

Vallender Tammy W TW Lahn Bruce T BT

FEBS letters 20060714 18

DNA methylation can contribute to the stable transcriptional silencing of mammalian genes. Often times, these genes are important developmental regulators, and their silencing in cell types where they are not supposed to be active is important for the phenotypic stability of the cells. To identify key developmental regulator genes whose expression in terminally differentiated cells may be inhibited by DNA methylation, mouse dermal fibroblasts were demethylated with 5-aza-2'-deoxycytidine, and ch ...[more]

PMID: 16870175

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Transcription profiling of primary mouse dermal fibroblasts, chondrocytes and osteoblasts treated with 5-aza-2?-deoxycytidine for 96/72h to identify key developmental regulator genes whose expression in terminally differentiated cells may be inhibited by DNA methylation

Project description:DNA methylation can contribute to the stable transcriptional silencing of mammalian genes. Oftentimes, these genes are important developmental regulators, and their silencing in cell types where they are not supposed to be active is important for the phenotypic stability of the cells. To identify key developmental regulator genes whose expression in terminally differentiated cells may be inhibited by DNA methylation, mouse dermal fibroblasts were demethylated with 5-aza-2-deoxycytidine, and changes in gene expression monitored by microarray analysis. Three biological replicates for both control and 5-aza-2'-deoxycytidine treatment were derived. Cells were primary mouse dermal fibroblasts, primary mouse chondrocytes, and primary mouse osteoblasts derived separately for each biological replicate. Treated cells were exposed to 5uM 5-aza-2'-deoxycytidine for 96 hours with recovery in normal medium for 24 hours. Control cells were untreated.

2007-11-23 | E-GEOD-4768 | biostudies-arrayexpress

Transcription profiling of mouse primary dermal fibroblasts treated with the de-methylating agent 5-aza-2?-deoxycytidine vs untreated to investigate methylation related changes in gene expression

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2007-11-23 | E-GEOD-4696 | biostudies-arrayexpress

Transcription profiling of mouse primary dermal fibroblasts treated with DNA demethylating agent 5-aza-2-deoxycytidine and sorted by X-chromosome-linked GFP expression

Project description:Primary mouse dermal fibroblasts from heterozygous female X chromosome-linked GFP mice were sorted through FACS for GFP non-expressing cells (~50% of cells due to X-inactivation). The GFP- cells were treated with 4uM 5-aza-2'-deoxycytidine (5A2dC) for 48 hours with recovery in normal medium for 24 hours. Following the treatment, cells were again sorted by FACS into GFP-activated and GFP-nonexpressing cells. These populations, along with a control untreated population were assayed for transcriptional changes by microarray.

2005-01-01 | E-MEXP-704 | biostudies-arrayexpress

Transcription profiling of mouse dermal fibroblasts from X linked GFP transgenics - improved dna methylation analysis via enrichment of demethylated cells expressing an X-inactivated GFP transgene

Project description:The demethylating drug 5-aza-2â-deoxycytidine (5-aza-2dC) is frequently used to investigate the; effect of global DNA demethylation on gene expression in cultured mammalian cells. Here, we utilize a novel method that uses the reactivation of an X-inactivated GFP transgene as a marker to enrich for cells that have undergone drug-induced demethylation. By combining it with microarray gene expression profiling, we demonstrate the methodâs utility in identifying genes activated by global DNA demethylation. Experiment Overall Design: Mice used have an X-linked GFP transgene driven by the chicken Î²-actin promoter and CMV Experiment Overall Design: intermediate early enhancer in a 129/ICR mixed genetic background obtained from The Jackson Experiment Overall Design: Laboratory. Male transgenic animals were bred to wildtype BL6 female mice to obtain females that were heterozygous for the transgene. Dermal fibroblasts were obtained from explant cultures of neonatal female mice from these crosses. The cells were then sorted using FACS to obtain only GFP-nonexpressing cells. These cells represent the population with the GFP transgene on the inactive X chromosome. The GFP-silent cells were treated with the demethylating drug 5-aza-2'-deoxycytidine. This drug does not affect all cells and uses a passive form of demethylation that results in a heterogenous population of unaffected and demethylated cells. A portion of the cells affected by demethylation activate the inactive GFP transgene by demethylating the inactive X chromosome. The GFP-active and GFP-inactive cells were sorted by FACS and assayed by microarray to determine what genes were affected by demethylation. Also the microarray results indicated if sorting for GFP-active cells enriches for cells affected by the drug.

2008-06-13 | E-GEOD-4718 | biostudies-arrayexpress

Transcription profiling of mouse primary dermal fibroblasts treated with endothelin-1

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2005-01-01 | E-MEXP-700 | biostudies-arrayexpress

Transcriptional analysis of pre and post excision human induced pluripotent stem cells

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2013-07-13 | E-GEOD-48830 | biostudies-arrayexpress

Transcription profiling of mouse dermal fibroblasts following exposure to endothelin-1

Project description:To determine if aberrant activation of endothelin-1 (Et1) could lead to the dysregulation of many downstream genes, we exposed fibroblasts to exogenous ET1 peptide and assayed for transcriptional changes by microarray. Mouse dermal fibroblasts were treated with exogenous Et1 peptide for 24 hours. ET1 treatment resulted in significant expression changes - primarily downregulation - of a number of genes. In particular, Tgf-beta-2 and Tgf-beta-3 were among the downregulated genes, which in turn alter the expression status of their many target genes. These data suggest that the stable silencing of Et1 is important for the phenotypic stability of dermal fibroblasts, and perhaps many other cell types as well.<br><br>Three separate biological replicates were derived for both control and treated samples. The primary dermal fibroblasts were derived by explant procedure from the skin of mouse pups aged 0-3 days. By passage 5, cells were split to two separate cultures-- one with 100nM synthetic Et1 peptide added to the medium (treated) and the other with nothing added (control). Cells were exposed to Et1 for 24 hrs, then treated and control populations were harvested for total RNA.

2007-06-29 | E-GEOD-4695 | biostudies-arrayexpress

Transcription profiling of rat fibroblasts transformed with HRAS and treated with the demethylating agent 5-aza-2-deoxycytidine

Project description:Silencing of gene expression by methylation of CpG islands in regulatory elements is frequently observed in cancer. However, an influence of the most common oncogenic signalling pathways onto DNA methylation has not yet been investigated thoroughly. To address this issue, we identified genes suppressed in HRAS-transformed rat fibroblasts but up-regulated after treatment with the demethylating agent 5-Aza-CdR and with the MEK1,2 inhibitor U0126. Analysis of gene expression by microarray and Northern blot analysis revealed the MEK/ERK target genes clusterin, Mmp2, Ppicap, syndecan 4, Timp2, Thbs1 to be repressed in the HRAS-transformed FE-8 cells in a MEK/ERK- and in a methylation-dependent manner. Hypermethylation of putative regulatory elements in HRAS-transformed cells as compared to immortalized fibroblasts was detected within a CpG island 14.5 kb upstream of clusterin, within the clusterin promoter and within a CpG island of the Mmp2 promoter by bisulphite sequencing. Furthermore, hypermethylation of the clusterin promoter was observed ten days after induction of HRAS in immortalized rat fibroblasts and a clear correlation between reduced clusterin expression and hypermethlyation could also be observed in distinct rat tissues. These results suggest that silencing of individual genes by DNA methylation is controlled by oncogenic signalling pathways, yet the mechanisms responsible for initial target gene suppression are variable. Experiment Overall Design: Gene expression was analyzed in immortal (208F) and HRAS oncogene-transformed (FE8) rat fibroblasts after demethylation by 5-aza-2'-deoxycytidine. Genes potentially methylated in RAS-transformed cells were identified by bisulphite sequencing

2007-11-06 | E-GEOD-4427 | biostudies-arrayexpress

Gene expression changes following demethylation by 5-aza-2'-deoxycytidine in primary mouse dermal fibroblasts

2006-04-25 | GSE4696 | GEO

Genome wide expression profiling of mesenchymal stem cells of fetal and adult origin and dermal fibroblasts

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