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Chip-chip from undifferentiated and neuron-differentiated hMSCs cells with EZH2

ABSTRACT: EZH2 plays an important role in stem cell renewal and maintenance by inducing gene silencing via its histone methyltransferase activity. Previously, we showed EZH2 downregulation markedly enhances neuron differentiation of human mesenchymal stem cells (hMSCs). To understand how EZH2 regulates neuron differentiation of hMSCs, we wanted to identify the target genes of EZH2. For this reasons we performed ChIP-on-chip experiments using specific EZH2 antibodies followed by a human promoter array for the whole human genome.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42686 | GEO | 2012/12/05

SECONDARY ACCESSION(S): PRJNA182909

REPOSITORIES: GEO

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Chip-chip from undifferentiated and neuron-differentiated hMSCs cells with EZH2

Project description:EZH2 plays an important role in stem cell renewal and maintenance by inducing gene silencing via its histone methyltransferase activity. Previously, we showed EZH2 downregulation markedly enhances neuron differentiation of human mesenchymal stem cells (hMSCs). To understand how EZH2 regulates neuron differentiation of hMSCs, we wanted to identify the target genes of EZH2. For this reasons we performed ChIP-on-chip experiments using specific EZH2 antibodies followed by a human promoter array for the whole human genome. The 3A6-hMSCs were differentiated into neuron for 5 days, and then 109 cells were harvested for the ChIP-on-chip assay. The procedure was based on the manufacturer's instructions (NimbleGen).

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2014-06-23 | E-GEOD-52563 | biostudies-arrayexpress

Effect of depletion of CTR9 on gene expression during early osteogenic differentiation of human primary mesenchymal stem cells

Project description:Cell-fate determination of human mesenchymal stem/stromal cells (hMSCs) is precisely regulated by lineage-specific transcription factors and epigenetic enzymes. We found that CTR9, a key scaffold subunit of Polymerase Associated Factor Complex (PAFc), selectively regulates hMSC differentiation to osteoblasts and chondrocytes, but not to adipocytes. An in vivo ectopic osteogenesis assay confirmed the essentiality of CTR9 in hMSC-derived bone formation. CTR9 counteracts the activity of EZH2, the epigenetic enzyme that deposits H3K27me3, in hMSCs. Accordingly, CTR9 knockdown (1) hMSCs gain H3K27me3 mark, and the osteogenic differentiation defects of CTR9 KD hMSCs can be partially rescued by treatment with EZH2 inhibitors. Transcriptome analyses identified Bone Morphology Protein-2 (BMP-2) as a downstream effector of CTR9. BMP-2 secretion, membrane anchorage, as well as the BMP-SMAD pathway were impaired in CTR9 KD MSCs, and the effects were rescued by BMP-2 supplementation. This study uncovers an epigenetic mechanism engaging CTR9-H3K27me3-BMP-2 axis to regulate osteochondral lineage differentiation of hMSCs. To investigate the function of CTR9 in the gene regulation of early osteogenic committment , we established human MSCs in which CTR9 gene has been knocked down by two individual shRNAs (shControl vs shCTR9#3/#5）.

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