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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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Tammy Vallender

PROVIDER: E-GEOD-4768 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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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