Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Comparative gene expression profiles induced by PPARM-NM-3 and PPARM-NM-1/M-NM-3 agonists in human hepatocytes

ABSTRACT: Transcriptomic profiling of primary human hepatocytes after treatment with 2 glitazones (TRO and ROSI) and 2 glitazars (MURA and TESA) Singe-Channel Samples: We have analysed changes in gene expression profiles in primary human hepatocytes after a 24 h treatment with various concentrations of glitazones and glitazars Dual-Channel Samples: We have analysed changes in gene expression profiles in primary human hepatocytes and differentiated human hepatoma HepaRG cells after a 24 h treatment with various concentrations of glitazones and glitazars Singe-Channel Samples: 5 condition experiments, control, TRO (3 concentrations) , ROSI (3 concentrations) , MURA (3 concentrations) and TESA (1 concentration) , biological replicates:2 to 4 Dual-Channel Samples: 5 condition experiments, control, TRO (3 concentrations) , ROSI (4 concentrations) , MURA (4 concentrations) and TESA (1 concentration) , biological replicates: 3

ORGANISM(S): Homo sapiens

SUBMITTER: rogue alexandra

PROVIDER: E-GEOD-27183 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:The transcription factor Peroxisome Proliferator-Activated Receptor M-NM-1 (PPARM-NM-1) is an important regulator of hepatic lipid metabolism. While PPARM-NM-1 is known to activate transcription of numerous genes, no comprehensive picture of PPARM-NM-1 binding to endogenous genes has yet been reported. To fill this gap, we performed ChIP-chip in combination with transcriptional profiling on HepG2 human hepatoma cells treated with the PPARM-NM-1 agonist GW7647. We found that GW7647 increased PPARM-NM-1 binding to 4220 binding regions. GW7647-induced binding regions showed a bias around the transcription start site and most contained a predicted PPAR binding motif. Several genes known to be regulated by PPARM-NM-1, such as ACOX1, SULT2A1, ACADL, CD36, IGFBP1 and G0S2, showed GW7647-induced PPARM-NM-1 binding to their promoter. A GW7647-induced PPARM-NM-1-binding region was also assigned to SREBP-targets HMGCS1, HMGCR, FDFT1, SC4MOL, and LPIN1, expression of which was induced by GW7647, suggesting cross-talk between PPARM-NM-1 and SREBP signaling. Our data furthermore demonstrate interaction between PPARM-NM-1 and STAT transcription factors in PPARM-NM-1-mediated transcriptional repression, and suggest interaction between PPARM-NM-1 and TBP and C/EBPM-NM-1 in PPARM-NM-1-mediated transcriptional activation. Overall, our analysis leads to important new insights into the mechanisms and impact of transcriptional regulation by PPARM-NM-1 in human liver and highlight the importance of cross-talk with other transcription factors. HepG2 cells were grown in phenol red-free DulbeccoM-bM-^@M-^Ys modified medium (DMEM) supplemented with 10% fetal bovine serum (FBS), 2 mM L-glutamine, 0.1 mg/ml streptomycin and 100 U/ml penicillin. Cells were split the day before experiments. Cells were kept at 37 M-BM-0C and 5% CO2. The following day, cells were treated with either 100 nM of the PPARM-NM-1 agonist GW7647 or control vehicle (DMSO). Cells used for gene expression analysis were harvested after 6 h or 24 h of GW7647 treatment. This submission represents the gene expression component of the study.

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Comparative gene expression profiles induced by PPARM-NM-3 and PPARM-NM-1/M-NM-3 agonists in human hepatocytes

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