Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse esophageal squamous cells after zinc-deficient or zinc-sufficient diet

ABSTRACT: Weanling littermates Cox-2-/- and Cox-2+/+ (WT) mice were fed a zinc-deficient (ZD) or zinc-sufficient (ZS) diet to form 4 groups, namely, ZD:Cox-2-/- (n=4), ZD:WT (n=4), ZS:Cox-2-/- (n=4) and ZS:WT (n=4). After 8 weeks, ZD mouse forestomach evidenced increased cell proliferation as demonstrated by increased proliferating cell nuclear antigen [PCNA] labeling. The mice were sacrificed and forestomachs isolated. Forestomach epithelia were prepared by using a blade to strip off the submucosal and muscularis layers under the guidance of a dissecting microscope. We performed microarray analysis on individual RNA samples prepared from 4 mice from each of the following 4 groups: ZS:Cox-2-/-, ZS:WT, ZD:Cox-2-/- and ZD:WT mice (n=4/group), using GeneChipï¾® Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA). All RNA samples displayed intact ribosomal RNA 18S and 28S bands as determined by the Agilent 2100 Bioanalyzer. Five micrograms of total RNA was reverse transcribed into cDNA followed by in vitro transcription and labeling to produce biotin-labeled cRNA using IVT Labeling Kit. The labeled cRNA was hybridized to the array, followed staining with streptavidin-phycoerythrin. The distribution of fluorescent material on the oligonucleotide probes sets was obtained using GeneArray Scanner

ORGANISM(S): Mus musculus

SUBMITTER: Cristian Taccioli

PROVIDER: E-TABM-778 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Zinc replenishment reverses overexpression of the proinflammatory mediator S100A8 and esophageal preneoplasia in the rat.

Taccioli Cristian C Wan Shao-Gui SG Liu Chang-Gong CG Alder Hansjuerg H Volinia Stefano S Farber John L JL Croce Carlo M CM Fong Louise Y Y LY

Gastroenterology 20081124 3

<h4>Background & aims</h4>Zinc deficiency is implicated in the pathogenesis of human esophageal cancer. In the rat esophagus, it induces cell proliferation, modulates genetic expression, and enhances carcinogenesis. Zinc-replenishment reverses proliferation and inhibits carcinogenesis. The zinc-deficient rat model allows the identification of biological differences affected by zinc during early esophageal carcinogenesis.<h4>Methods</h4>We evaluated gene expression profiles of esophageal epitheli ...[more]

PMID: 19111725

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Project description:Zinc is an essential nutrient because of its role in catalysis and in stabilizing protein structure, but excess zinc can also be deleterious. Four nutritional zinc states have been identified in the alga Chlamydomonas reinhardtii: zinc toxic, zinc replete, zinc deficient and zinc limited. Growth is inhibited in zinc-limited and zinc toxic cells relative to zinc-replete cells, while zinc-deficiency is visually asymptomatic but distinguished by the accumulation of transcripts encoding ZIP family transporters. To identify targets of zinc deficiency and mechanisms of zinc acclimation, we used RNA-seq to probe zinc nutrition responsive changes in gene expression. We identified a subset of genes encoding zinc-handling components, including ZIP family transporters and candidate zinc chaperones. In addition, we noted an impact on two other regulatory pathways, the carbon concentrating mechanism (CCM) and the nutritional copper regulon. Targets of transcription factor Ccm1 and various CAH genes are up-regulated in zinc-deficiency, as a likely consequence of reduced carbonic anhydrase activity, which is validated by mass spectrometry and immunoblot analysis of Cah1, Cah3 and Cah4. Chlamydomonas is therefore not able to grow photoautotrophically in air in zinc limiting conditions, but supplementation with 1% CO2 restores growth to wild-type rates, suggesting that the inability to maintain CCM is a major consequence of zinc limitation. Surprisingly, we noted also that the Crr1 regulon, which responds to Cu limitation, is also turned on in zinc deficiency, and in fact, Crr1 is required for growth in zinc-limiting conditions. Zinc deficient cells are functionally copper deficient, as evidenced by reduced plastocyanin abundance, even though they hyperaccumulate copper up to 50-fold over normal levels. We suggest that zinc-deficient cells sequester Cu in a bio-unavailable form, perhaps to prevent mis-metallation of critical zinc sites. Zn-limited wild-type cells were generated by transfer of cells from the first round of growth in medium with no supplemental Zn into TAP medium supplemented or not with 2.5 ÂµM Zn-EDTA The control samples for this study are represented in GSE25622

Dataset Information

Transcription profiling of mouse esophageal squamous cells after zinc-deficient or zinc-sufficient diet

Publications

Zinc replenishment reverses overexpression of the proinflammatory mediator S100A8 and esophageal preneoplasia in the rat.

Similar Datasets

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