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University of California-San Diego: Dataset Details, ID=GSE41579

Superfund Research Program

Toxicogenomic Analysis of Nuclear Xenobiotic Receptors

Project Leader: Ronald M. Evans (Salk Institute for Biological Studies)
Grant Number: P42ES010337
Funding Period: 2005-2017
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Title: A master cistromic circuit governing hepatic fibrogenesis [expression array]

Accession Number: GSE41579

Link to Dataset: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41579

Repository: Gene Expression Omnibus (GEO)

Data Type(s): Gene Expression

Experiment Type(s): Expression profiling by array

Organism(s): Rattus norvegicus

Summary: Liver fibrosis is a reversible wound-healing response to liver injury and hepatic stellate cells (HSCs) are central cellular players that mediate hepatic fibrogenesis. However, the molecular mechanisms that govern this process remain unclear. Expression profiling was used to explore the potential impact of VDR signaling in TGF 1 and TGF 1+1,25(OH)2D3-treated primary rat HSCs. Notably, 1,25(OH)2D3 treatment attenuated the culture-induced activation of HSCs, such that the transcriptome of treated cells closely resembled that of freshly isolated quiescent cells (Figure 2A), and co-treatment of 1,25(OH)2D3 together with TGF resulted in considerable repression of a large set of TGF induced genes. We also demonstrated that in primary mouse HSCs, calcipotriol potently repressed fibrotic gene expression, suggesting that the anti-TGF properties of VDR agonists are likely conserved across mammalian species.

Publication(s) associated with this dataset:
  • Ding N, Yu RT, Subramaniam N, Sherman MH, Wilson C, Rao R, Leblanc M, Coulter S, He M, Scott C, Lau SL, Atkins AR, Barish GD, Gunton JE, Liddle C, Downes M, Evans RM. 2013. A vitamin D receptor / SMAD genomic circuit gates hepatic fibrotic response. Cell 153(3):601-613. doi:10.1016/j.cell.2013.03.028 PMID:23622244 PMCID:PMC3673534
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