Project description:We report the RNA-sequencing analysis of hepatic RNA isolated from CD-1 mice following gestational exposure to 500ppb CdCl2. We show that gestational Cd exposure alters the hepatic gene expression of female, but not male offspring in numerous pathways related to oxidative stress and mitochondrial dysfunction leading to endoplasmic reticulum stress that ultimately drives metabolic disruption of insulin signaling.
Project description:In this study we want to compare the gene expression profile of CD44+CXCR6+ CD8+ T cells from the liver of ND and CD-HFD mice with hepatic CD44+CXCR6neg and splenic CD44+ CX3CR1neg CD8 T cells of ND and CD-HFD mice. This comparison will reveal transcriptional signatures of hepatic CD44+CXCR6+ CD8+ T cells in CD-HFD responsible for causing liver pathology in NASH.
Project description:The goal of this study was to apply transcriptional analyses to hepatic tissues from mice exposed to PB, propiconazole (Pro) or triadimefon (Tri) at tumorigenic exposure levels to reveal similarities and differences in response among these treatments.The goal of this study was to apply transcriptional analyses to hepatic tissues from mice exposed to PB, propiconazole (Pro) or triadimefon (Tri) at tumorigenic exposure levels to reveal similarities and differences in response among these treatments. Experiment Overall Design: Briefly, male CD-1 mice received propiconazole (2500 ppm), tridimefon (1800 ppm), or phenobarbital (850 ppm) in the feed or, control feed for periods of 4 and 30 days. This resulted in an average daily intake of 349.6 ± 46.7 of propiconazole, 257.1 ± 33.5 of tridimefon or 97.2 ± 5.9 mg/kg/day of phenobarbital.
Project description:Cadmium (Cd) is a toxic metal causing sublethal and chronic effects in crustaceans. Omic technologies offer unprecedented opportunities to better understand modes of toxicity by providing a holistic view of the molecular changes underlying physiological disruption. We sought to use gene expression and metabolomic analyses to reveal the processes leading to chronic Cd toxicity in the indicator species, Daphnia magna, after a 24-h sublethal exposure (18 ug/L, corresponding to 1/10 LC50). We first confirmed that metabolites can be detected and identified in small volumes (~3-6 ul) of D. magna hemolymph using Fourier transform ion cyclotron resonance (FT-ICR) mass spectrometry and NMR spectroscopy. We then compared the altered metabolite levels from a mass spectrometry metabolomics study to differentially expressed genes identified by a D. magna 44k oligonucleotide microarray. Metabolomics identified several essential amino acids, nucleotides and fatty acids as decreased in D. magna hemolymph following Cd exposure. Transcriptional changes included decreased levels of digestive enzymes and increased expression of genes related to embryonic development. The integration of metabolomic and transcriptomic profiles, as well as incorporation of results from previous studies, has enabled construction of a conceptual model detailing how sublethal Cd disrupts energy reserves and reproduction resulting in chronic toxicity. Daphnia magna were exposed to 18 micrograms/L Cadmium sulfate for 24 hours. RNA was extracted and hybridized to a custom Daphnia magna microarray to determine genes differentially expressed by the treatment. Two treament experiment:Unexposed and Cd treatment, 6 replicates for each condition
Project description:Gene expression can vary with the organisms' life stage. It is known that embryos can be more sensitive to toxicant exposure, as previously demonstrated for Enchytraeus crypticus (Oligochaeta) exposed to cadmium (Cd), known to cause embryotoxicity and hatching delay. It was shown that Ca enters embryos via the L-type Ca channels in the cocoon membrane, this being affected in Cd exposed embryos (Cd-Ca competition is well-known). In the present study, the embryotoxic mechanisms of Cd were studied via high-throughput gene expression for E. crypticus. Cocoons (1e2 days old), instead of the adult organism, were exposed in Cd spiked LUFA 2.2 soil during 1 day. Results showed that Cd affected Ca homeostasis which is implicated in several other molecular processes. Several of the major modulators of Cd toxicity (e.g., impaired gene expression, cell cycle arrest, DNA and mitochondrial damage) were identified in the embryos showing its relevancy as a model in ecotoxicogenomics. The draft Adverse Outcome Pathway was improved. Previously was hypothesized that gene regulation mechanisms were activated to synthesize more Ca channel proteins e this was confirmed here. Further, novel evidences were that, besides the extracellular competition, Cd competes intracellularly which causes a reduction in Ca efflux, and potentiates Cd embryotoxicity.
Project description:The heavy metal cadmium (Cd) accumulates in the environment due to anthropogenic influences. It is unessential and harmful to all life forms. The plant cell wall forms a physical barrier against environmental stress and changes in the cell wall structure have been observed upon Cd exposure. In the current study, changes in the cell wall composition and structure of Medicago sativa stems were investigated after long-term exposure to Cd. Liquid chromatography coupled to mass spectrometry (LC-MS) for quantitative protein analysis was complemented with targeted gene expression analysis and combined with analyses of the cell wall composition. Compared to most studies the plants were exposed to the heavy metal for an entire season, including the repeated cutting of the above-ground biomass as is done in agriculture.
Project description:To reveal the molecular mechanism underlying EIN3-mediated Cd tolerance, we performed RNA sequencing (RNA-seq) analysis to identify Cd-regulated genes that are differentially expressed in ein3 eil1 double mutant.