Gene expression profiling reveals potential breast cancer prevention mechanisms associated with the rat Mcs5a allele (DGE)
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE33975 | GEO | 2011/11/29
SECONDARY ACCESSION(S): PRJNA150511
REPOSITORIES: GEO
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2011-11-29 | E-GEOD-33975 | biostudies-arrayexpress
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Project description:To compare the tumor susceptibility between the hypertensive Dahl salt-sensitive rats (S) rat and S.LEW(10)x12x2x3x5 (S.LEW) congenic strain, one of the S.LEW congenic strains our laboratory previously constructed on rat chromosome 10 [Hypertension. 2007 Nov;50(5):891-8], Azoxymethane (AOM)-induced colon tumorigenesis in rats was assessed. At six weeks of age, both S and S.LEW congenic rats received intraperitoneal (IP) injection of AOM in sterial saline at a dose of 15mg/kg body weight once a week for two consecutive weeks. At 30 weeks of age, all the rats were euthanized through carbon dioxide inhalation. The colon tissue was harvested, dissected longitudinally, and washed with saline. The number and size of the colon tumors were recorded. We found that the total number of colon tumors was significantly higher in the S.LEW congenic strain compared with the S rat. To further study the genetic and molecular mechanisms causing the higher tumor susceptibility in the S.LEW congenic strain, we have employed the whole genome microarray expression profiling to identify genes and signaling pathways that are differential between the S and S.LEW congenic strain.
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Project description:We are using the ACI rat model of 17beta-estradiol induced mammary cancer to define the mechanisms through which estrogens contribute to breast cancer development; identify and functionally characterize the genetic variants that determine susceptibility; and define the hormone-gene-environment interactions that influence development of mammary cancer in this physiologically relevant rat model. Female ACI rats are uniquely susceptible to development of mammary cancer when treated continuously with physiologic levels of 17beta-estradiol. Induction of mammary cancer in female ACI rats occurs through a mechanism that is largely dependent upon estrogen receptor-alpha. Interval mapping analyses of progeny generated in intercrosses between susceptible ACI rats and resistant Brown Norway (BN) rats revealed seven quantitative trait loci (QTL), designated Emca3 (Estrogen-induced mammary cancer) through Emca9, each of which harbors one or more genetic determinants of mammary cancer susceptibility. Genes that reside within Emca8 on RNO5 and were differentially expressed between 17beta-estradiol treated ACI and ACI.BN-Emca8 congenic rats were identified as Emca8 candidates.
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Project description:Background and Aims: In the interleukin-10-deficient (Il10-/-) mouse model of IBD, 10 quantitative trait loci (QTL) have been shown to be associated with colitis susceptibility by linkage analyses on experimental crosses of highly susceptible C3H/HeJBir (C3Bir)-Il10-/- and partially resistant C57BL/6J (B6)-Il10-/- mice. The strongest locus (C3Bir-derived cytokine deficiency-induced colitis susceptibility [Cdcs]1 on Chromosome [Chr] 3) controlled multiple colitogenic subphenotypes and contributed the vast majority to the phenotypic variance in cecum and colon. This was demonstrated by interval-specific Chr 3 congenic mice wherein defined regions of Cdcs1 from C3Bir or B6 were bred into the IL-10-deficient reciprocal background and altered the susceptible or resistant phenotype. Furthermore, this locus likely acts by inducing innate hypo- and adaptive hyperresponsiveness, associated with impaired NFΚB responses of macrophages. The aim of the present study was to dissect the complexity of Cdcs1 by further development and characterization of reciprocal Cdcs1 congenic strains and to identify potential candidate genes in the congenic interval. Material and Methods: In total, 15 reciprocal congenic strains were generated from Il10-/- mice of either C3H/HeJBir or C57BL/6J backgrounds by 10 cycles of backcrossing. Colitis activity was monitored by histological grading. Candidate genes were identified by fine mapping of congenic intervals, sequencing, microarray analysis and a high-throughput real-time RT-PCR approach using bone marrow-derived macrophages. Results: Within the originally identified Cdcs1-interval, three independent regions were detected that likely contain susceptibility-determining genetic factors (Cdcs1.1, Cdcs1.2, and Cdcs1.3). Combining results of candidate gene approaches revealed Fcgr1, Cnn3, Larp7, and Alpk1 as highly attractive candidate genes with polymorphisms in coding or regulatory regions and expression differences between susceptible and resistant mouse strains. Conclusions: Subcongenic analysis of the major susceptibility locus Cdcs1 on mouse chromosome 3 revealed a complex genetic structure. Candidate gene approaches revealed attractive genes within the identified regions with homologs that are located in human susceptibility regions for IBD. Experiment Overall Design: Bone marrow derived macrophages (BMDM) of colitis susceptible C3Bir-Il10-/- and colitis resistant B6-Il10-/- as well as the Il10-/- reciprocal congenic strains CB-R1 (C3Bir genetic background carrying a long congenic chromosome 3 element containing Cdcs1 from B6, rendering this formerly susceptible background resistant) and BC-R3 (B6 genetic background that carries the Cdcs1-region of C3Bir) were cultured and stimulated with flagellin or left unstimulated. BMDM were obtained from 3 male mice per genotype and cultured in polystyrene 6-well culture plates. Before RNA-isolation, 3 wells per plate were stimulated with Cbir1 flagellin (and subsequently pooled for RNA isolation), the other 3 wells left unstimulated (and also pooled). In total, these experiments were replicated three times in order to perform microarray analyses in triplicates.
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Project description:Anterior pituitary glands were isolated from 21 week old male rats treated for 12 weeks with the synthetic estrogen diethylstilbestrol (DES). Three biological replicates were prepared for each of 4 congenic lines: Ept1, Ept2, Ept6, and Ept9. Congenic rat lines were constructed by introgressing COP alleles onto an ACI background within a given Ept locus. Expression profiles were determined using Affymetrix Rat Genome 230 v. 2.0 arrays. Comparison of congenic rats with the ACI and COP parental strains (see series GSE4028) will allow identification of genes whose expression is influenced by an estrogen-induced pituitary tumor (Ept) QTL. Keywords: Estrogen Response
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