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Series GSE13513 Query DataSets for GSE13513
Status Public on Nov 14, 2011
Title Patterns of dioxin-altered mRNA expression in livers of dioxin-sensitive versus dioxin-resistant rats
Organism Rattus norvegicus
Experiment type Expression profiling by array
Summary The dioxin congener 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes a wide range of toxic effects in rodent species, all of which are mediated by a ligand-dependent transcription-factor, the aryl hydrocarbon receptor (AHR). The Han/Wistar (Kuopio) (H/W) strain shows exceptional resistance to many TCDD-induced toxicities; the LD50 of >9600 µg/kg for H/W rats is higher than for any other wild-type mammal known. We have previously shown that this resistance primarily results from H/W rats expressing a variant AHR isoform that has a substantial portion of the AHR transactivation domain deleted. Despite this large deletion, H/W rats are not entirely refractory to the effects of TCDD; the variant AHR in these animals remains fully competent to up-regulate well-known dioxin-inducible genes. TCDD-sensitive (Long-Evans, L-E) and resistant (H/W) rats were treated with either corn-oil (with or without feed-restriction) or 100 µg/kg TCDD for either four or ten days. Hepatic transcriptional profiling was done using microarrays, and was validated by RT-PCR analysis of 41 genes. . A core set of genes was altered in both strains at all time points tested, including CYP1A1, CYP1A2, CYP1B1, Nqo1, Aldh3a1, Tiparp, Exoc3, and Inmt. Outside this core, the strains differed significantly in the breadth of response: three-fold more genes were altered in L-E than H/W rats. At ten days almost all expressed genes were dysregulated in L-E rats, likely reflecting emerging toxic responses. Far fewer genes were affected by feed-restriction, suggesting that only a minority of the TCDD-induced changes are secondary to the wasting syndrome.
Overall design Rats from sensitive (Long-Evans, LE) and resistant (Han/Wistar, HW) strains were treated with 100 ug/kg TCDD or corn oil vehicle and sacrificed either 4 or 10 days after treatment. LE control rats were either fed normally or feed-restricted to control for the wasting effects of TCDD treatment. Each treatment group contains four or five animals (biological replicates), each of which was assayed on an individual microarray.
Contributor(s) Boutros PC, Yao CQ, Watson JD, Wu AH, Moffat ID, Prokopec SD, Smith AB, Okey AB, Pohjanvirta R
Citation(s) 21215274
Submission date Nov 07, 2008
Last update date Mar 20, 2012
Contact name Paul C Boutros
Organization name Ontario Institute for Cancer Research
Street address 101 College Street, Suite 800
City Toronto
State/province Ontario
ZIP/Postal code M5G 0A3
Country Canada
Platforms (1)
GPL9199 Affymetrix GeneChip Rat Genome 230 2.0 Array (CDF: Rat2302_Rn_ENTREZG.cdf version 12.0.0)
Samples (45)
GSM340813 Rat liver LE TCDD 10 days rep1
GSM340814 Rat liver LE TCDD 10 days rep2
GSM340815 Rat liver LE TCDD 10 days rep3
BioProject PRJNA110117

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SOFT formatted family file(s) SOFTHelp
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Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE13513_RAW.tar 2.3 Gb (http)(custom) TAR (of CEL, DAT)
Processed data included within Sample table

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