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Project description:Arsenic (As) exposure is a significant worldwide environmental health concern. Low dose, chronic arsenic exposure has been associated with higher risk of skin, lung, and bladder cancer, as well as cardiovascular disease and diabetes. While arsenic-induced biological changes play a role in disease pathology, little is known about the dynamic cellular changes due to arsenic exposure and withdrawal. In these studies, we seek to understand the molecular mechanisms behind the biological changes induced by chronic low doses of arsenic exposure. We used a comprehensive approach involving chromatin structural studies and mRNA microarray analyses to determine how chromatin structure and gene expression patterns change in response to chronic low dose arsenic exposure and its subsequent withdrawal. Our results show that cells exposed to low doses of sodium arsenite have distinct temporal and coordinated chromatin, gene expression and miRNA changes that are consistent with differentiation and activation of multiple biochemical pathways. Most of these temporal patterns in gene expression are reversed when arsenic was withdrawn. However, some of the gene expression patterns remained altered, plausibly as a result of an adaptive response by these cells. Additionally, these gene expression patterns correlated with changes in chromatin structure, further solidifying the role of chromatin structure in gene regulatory changes due to arsenite exposure. Lastly, we show that arsenite exposure influences gene regulation both at the transcription initiation as well as at the splicing level. Thus our results suggest that general patterns of alternative splicing, as well as expression of particular gene regulators, can be indicative of arsenite-induced cell transformation. A total of eight (8) samples with two biological replicates under four separate conditions: wild-type treated with deionized H2O for 36 days (NT); chronic low-dose arsenic exposure of 1 uM of sodium arsenite (iAs-T) for 36 days; chronic arsenic exposure of 1 uM of sodium arsenite for 26 days followed by removal of sodium arsenite for 10 days, measured at day 36 (iAs-Rev); and chronic arsenic exposure of 1 uM of sodium arsenite for 26 days, followed by removal of sodium arsenite exposure for 10 days, followed by 1 uM of chronic sodium arsenite exposure for 10 days (measured at day 46) (iAs-Rev-T).
2015-05-05 | E-GEOD-60760 | biostudies-arrayexpress
Project description:RNA expression profiles are not significantly altered by DDX3 WT or R534H expression as well as by 45 minute exposure of cells to sodium arsenite.
2016-04-21 | GSE70803 | GEO
Project description:IP of 3xFLAG-TRAPPC2 in state state and under Sodium Arsenite to find interactor
2019-08-12 | PXD014395 | Pride
Project description:Microarray data from G2-synchronized p53(+) and p53(-) fibroblasts before and after 3 h release from cell cycle blockade in the presence of 5 µM sodium arsenite. Keywords: Gene induction
2007-04-07 | GSE7101 | GEO
Project description:Stress-induced tRNA fragmentation is an evolutionarily conserved molecular phenomenon. A variety of the resulting tRNA-derived small RNAs (tsRNAs) have been associated with a multitude of cellular processes including cell survival during adverse environmental conditions. However, application of experimental stressors under laboratory conditions often differs from stress encountered naturally. This raises important questions about the extent of experimental bias when studying stress biology including tRNA fragmentation, especially in cell culture. Here, we have revisited one of the most often used experimental paradigms for modeling oxidative stress and tRNA fragmentation, the exposure of cultured cells to sodium arsenite. These experiments revealed that transient exposure to sodium arsenite concentrations that caused robust tRNA fragmentation resulted in extensive cell death during the stress recovery. Importantly, released material from dying cells contained also tsRNA species, which were sufficiently stable against nuclease digestion.
2021-12-31 | GSE182334 | GEO
Project description:Exposure to high levels of arsenic in drinking water is associated with several types of cancers including lung, bladder and skin, as well as vascular disease and diabetes. Drinking water standards are based primarily on epidemiology and extrapolation from higher dose experiments, rather than measurements of phenotypic changes associated with chronic exposure to levels of arsenic similar to the current standard of 10ppb, and little is known about the difference between arsenic in food as opposed to arsenic in water. Measurement of phenotypic changes at low doses may be confounded by the effect of laboratory diet, in part because of trace amounts of arsenic in standard laboratory chows, but also because of broad metabolic changes in response to the chow itself. Finally, this series contrasts 8hr, 1mg/kg injected arsenic with the various chronic exposures, and also contrasts the acute effects of arsenic, dexamethasone or their combination. Male C57BL/6 mice were fed on two commercially available laboratory diets (LRD-5001 and AIN-76A) were chronically exposed, through drinking water or food, to environmentally relevant concentrations of sodium arsenite, or acutely exposed to dexamethasone. Experiment Overall Design: Male C57BL/6 mice, fed on two commercially available laboratory diets (LRD-5001 and AIN-76A), were chronically exposed through drinking water or food, to environmentally relevant concentrations of sodium arsenite. Another group animals, fed on the AIN 76A diet, was IP injected with dexamethasone (1 mg/kg), sodium arsenite (1mg/kg), both dexamethosone and arsenite, or saline alone.
2008-10-21 | E-GEOD-11056 | biostudies-arrayexpress
Project description:Purpose: To determine the effects of sodium arsenite in male mice on adaptive thermogenesis. Methods: Male C57BL/6J mice were exposed to sodium arsenite in drinking water at 300 parts per billion (ppb) for 9 weeks Findings: Arsenic-treated mice experienced significantly decreased metabolic heat production when acclimated to chronic cold tolerance testing, as evidenced by indirect calorimetry, despite no change in physical activity. Arsenic exposure increased total fat mass, and unilocular lipid droplet size in both subcutaneous inguinal white adipose tissue (iWAT) and brown adipose tissue (BAT). Conclusion: Chronic arsenic exposure impacts the mitochondria of thermogenic tissues involved in energy expenditure and glucose regulation, providing novel mechanistic evidence for arsenic’s role in metabolic pathologies.
2020-01-01 | GSE134982 | GEO
Project description:Microarray data from G2-synchronized p53(+) and p53(-) fibroblasts before and after 3 h release from cell cycle blockade in the presence of 5 uM sodium arsenite. Experiment Overall Design: Cells expressing p53 from a tet-off regulated construct were synchronized in G2 with a two-step procedure using 24 h aphidicolin treatment for initial G1 synchronization and 12 h of Hoechst 33342 to effect a G2 blockade. During Hoechst treatment, tetracycline was added to suppress p53 in half the cultures. Cells were then released into media containing 5 µM sodium arsenite and the appropriate concentration of tetracycline to maintaining p53 expression. mRNAs were collected at 0 h and 3 h after release from G2 synchrony.
2007-11-11 | E-GEOD-7101 | biostudies-arrayexpress
Project description:The transcriptional response of K. lactis yeast was investigated following exposure to sodium arsenite (As(III)) and tert-butyl hydroperoxide (t-BOOH). We compared the genome-wide expression profile of Klyap8∆ mutant cells to that of the wild type.
2014-10-06 | GSE55128 | GEO
Project description:Exposure to high levels of arsenic in drinking water is associated with several types of cancers including lung, bladder and skin, as well as vascular disease and diabetes. Drinking water standards are based primarily on epidemiology and extrapolation from higher dose experiments, rather than measurements of phenotypic changes associated with; chronic exposure to levels of arsenic similar to the current standard of 10ppb, and little is known about the difference between arsenic in food as opposed to arsenic in water. Measurement of phenotypic changes at low doses may be confounded by the effect of laboratory diet, in part because of trace amounts of arsenic in standard laboratory chows,; but also because of broad metabolic changes in response to the chow itself. Finally, this series contrasts 8hr, 1mg/kg injected arsenic with the various chronic exposures, and also contrasts the acute effects of arsenic, dexamethasone or their combination. Male C57BL/6 mice were fed on two commercially available laboratory diets (LRD-5001 and AIN-76A) were chronically exposed, through drinking water or food, to environmentally relevant concentrations of sodium arsenite, or acutely exposed to dexamethasone. Experiment Overall Design: Male C57BL/6 mice, fed on two commercially available laboratory diets (LRD-5001 and AIN-76A), were chronically exposed through drinking water or food, to environmentally relevant concentrations of sodium arsenite. Experiment Overall Design: Another group animals, fed on the AIN 76A diet, was IP injected with dexamethasone (1 mg/kg), sodium arsenite (1mg/kg), both dexamethosone and arsenite, or saline alone.
2008-06-16 | E-GEOD-9630 | biostudies-arrayexpress