Nuclear Receptor


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Gene expression profiling of potential peroxisome proliferator-activated receptor (PPAR) target genes in human hepatoblastoma cell lines inducibly expressing different PPAR isoforms

Keisuke Tachibana1, Yumi Kobayashi1, Toshiya Tanaka2, Masayuki Tagami1, Akira Sugiyama3,2, Tatsuya Katayama1, Chihiro Ueda1, Daisuke Yamasaki1, Kenji Ishimoto1, Mikako Sumitomo1, Yasutoshi Uchiyama3,2, Takahide Kohro2, Juro Sakai2, Takao Hamakubo2, Tatsuhiko Kodama2 and Takefumi Doi4,1*

Author Affiliations

1 Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan

2 Laboratory for System Biology and Medicine, The Research Center for Advanced Science and Technology, the University of Tokyo, Tokyo, Japan

3 Perseus Proteomics Inc, Tokyo, Japan

4 Graduate School of Medicine, Osaka University, Osaka, Japan

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Nuclear Receptor 2005, 3:3 doi:10.1186/1478-1336-3-3

Published: 3 October 2005

Additional files

Additional File 1:

Changes in mRNA expression levels in HepG2-tet-off-hPPAR cell lines by ligands. Microarray analyses were performed on HepG2-tet-off-hPPAR cells; the cells were cultured in the presence (Dox) or absence of Dox for 5 days. In the absence of Dox, the cells were treated with PPAR ligands (100 μM fenofibric acid for PPARα (Feno), 100 nM GW501516 for PPARδ (GW) or 10 μM ciglitizone for PPARγ (Cig)) or vehicle (DMSO) for 24 h. Gene expression profiles were compared between DMSO and Dox (DMSO versus Dox), ligands and Dox (Feno versus Dox, GW versus Dox, and Cig versus Dox were indicated in the case of PPARα, PPARδ and PPARγ, respectively) or ligands and DMSO (Feno versus DMSO, GW versus DMSO, and Cig versus DMSO were indicated in the case of PPARα, PPARδ and PPARγ, respectively). Average differences expressed the intensities of the mRNA levels in HepG2-tet-off-hPPARs cell lines. Samples were analysed using GeneChip® software Microarray Suite (MAS) Ver.5.0 (Affymetrix).

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