Expression data from murine hematopoietic stem cells isolated from mice treated with control oil or estradiol
ABSTRACT: The division rate of hematopoietic stem cells (HSCs) are promoted by estradiol. To identify the mechanism by which estradiol regulates HSCs, we performed gene expresssion profiling of HSCs isolated from mice of both sexes treated with either control vehicle (oil) or estradiol for one week. 4 groups were analyzed; 1) HSCs from male mice treated with oil, 2) HSCs from male mice treated with estradiol, 3) HSCs from female mice treated with oil, and 4) HSCs from female mice treated with estradiol. All groups include 3 biological replicates isolated from 3 mice.
Project description:To investigate the differences in microRNA expression profiles between fibrotic and normal livers, we performed microRNA microarrays for total RNA extracts isolated from mouse livers treated with carbontetrachloride (CCl4) or corn-oil for 10 weeks (n=3/group). MicroRNAs were considered to have significant differences in expression level when the expression difference showed more than two-fold change between the experimental and control groups at p<0.05. We found that 12 miRNAs were differentially expressed in CCl4-induced fibrotic liver. To induce chronic liver fibrosis, seven-week-old mice received 0.6 ml/kg body weight of carbon-tetrachloride (CCl4) dissolved in corn-oil by intraperitoneal (i.p.) injection, twice a week for 10 weeks (n=3). As a control, same number of mice was injected with equal volume of corn-oil for 10 weeks.
Project description:Provided later Pregnant Fisher 344 rats will be purchased from Charles River Laboratories, Inc. and delivered to CIIT on gestational day (GD) 7 (GD0 = day first vaginal plug positive). At gestational day 12 (GD12), the dams will be exposed once/day until GD20 to 50 mg/kg dibutyl phthalate (DBP) in corn oil vehicle via oral gavage. Each dose group will contain 4-6 vehicle control or phthalate treated dams. Groups of animals will be sacrificed at GD20, postnatal day (PND) 35, and PND90 for endpoint analysis. At GD20, treated and control animals will be examined for various endpoints including body weight, testicular histopathology, gene expression profile via microarray analysis, and anogenital distance (AGD). AGD (at parturition; PND1) and nipple number/location (at PND14 and day of sacrifice) will be determined on animals in the postnatal groups. At PND35 or 90, one male from each in utero corn oil vehicle or DBP exposed group will receive a second gavage of either corn oil or 500 mg/kg DBP. 6 hours after the second gavage, the following endpoints will be examined: 1) testis histopathology; 2) spermatid head quantification (PND90 only); 3) testis and body weights; 5) genome-wide gene expression (via microarray); and 6) germ cell apoptosis (TUNEL assay).
Project description:Hepatic stellate cells are involved in the development of hepatic fibrosis. We here perform transcriptional profiling of hepatic stellate cells (HSCs) isolated from Western diet/high fructose-fed C57BL6/J mice, carbon tretrachloride (CCl4)-treated C57BL6/J mice, and of murine HSCs differentiated in vitro. Specifically, gene expression profiles are obtained from hepatic stellate cells isolated from C57BL6 mice fed a Western Diet supplemented with high fructose for 12, 16 or 24 weeks or normal chow. From hepatic stellate cells isolated from C57BL6 mice treated CCl4 for 1, 4 or 8 weeks or treated with vehicle. From hepatic stellate cells isolated from healthy C57BL6 mice and seeded on normal plastic cell culture dishes for 1, 4, 8, or 12 days. And from hepatic stellate cells isolated from healthy C57BL6 mice and seeded on normal plastic cell culture dishes for 6 days in the presence of 10uM U0126 or DMSO.
Project description:Adult Sprague Dawley rats were treated i.g. with 50 mg/kg alpha-naphthylisothiocyanate (ANIT) or vehicle (corn oil). Hepatobiliary liver injury occurred at 24 h postdose in ANIT rats with repair at 120h. Livers were extracted from rats at 24h and 120 h post ANIT exposure. This study investigated differences in mRNA expression between the injury and repair phases in the context of ANIT exposure. 8 week male Sprague Dawley rats were administered ANIT or vehicle for quantification of hepatobiliary injury via clinical chemistry biomarkers and pathology between 6 and 168 h postdosing. Rats sacrificed at 24 h and 120h postdosing coincided with peak injury and injury resolution, respectively.
Project description:Immature (19/20 days of age) Alpk:APfCD-1 mice were treated with arachis oil (AO) vehicle or 0.4mg/kg 17beta-estradiol (E2), via a single subcutaneous injection, and sacrificed at 1hr, 2hr, 4hr, 8hr, 24hr, 48hr, 72hr post dose.
Project description:Five-week-old male mice (Mus musculus, ICR) were exposed to dechlorane plus for 10 days. A total of tweenty-four mice were randomly assigned to control and three DP-treated groups. Six mice were applied in every group. For control group, corn oil was given to mice by gavage daily. For three DP-treated groups, mice received a daily dose of DP in corn oil at 500 mg DP /kg bw, 2000 mg DP /kg bw and 5000 mg DP /kg bw, respectively. After exposure, mice were anaesthetized under isoflurane followed by exsanguination. Livers were removed, and hepatic RAN for each mouse were immediately extract. The gene expression profiles for control and three DP-treated groups were determined by the GeneChip? Mouse Exon 1.0 ST arrays. the biological significances of differentially expressed genes (DEGs) were analyzed based on Molecule Annotation System 3.0 (MAS3.0, http://bioinfo.capitalbio.com/mas/). The microarray analysis of this study provide novel insight regarding toxicological effects and mechanism of DP at the transcriptome level
Project description:Most commonly used models of non-alcoholic steatohepatitis (NASH) are diets based on specific gene knockouts or represent extreme manipulations of diet. We have examined the effects of modest increased caloric intake and high dietary unsaturated fat content on the development of NASH in male rats using a model in which overfeeding is accomplished via intragastric infusion of liquid diets as a part of total enteral nutrition. Male Sprague dawley rats were fed diets 5% corn oil containing diets at 187 Kcal/kg3/4/d or fed 70% corn oil containing diets at 220 Kcal/kg3/4/d for a period of 3 weeks. Hepatic gene expression were assessed at the end of the study. Our results indicate that overfeeding of high unsaturated fat diets leads to pathological, endocrine and metabolic changes characteristic of NASH patients and is associated with increased oxidative stress and TNF-a. Experiment Overall Design: Two groups of male sprague dawley rats were fed liquid diets via total enteral nutrition. Experiment Overall Design: Group 1, Control, Rats were fed diets containing 5% Corn oil at 187 Kcal/kg3/4/d for 3 weeks. Experiment Overall Design: Group 2, NASH, Rats were fed diets containing 70% corn oil at 220 Kcal/kg3/4/d for 3 weeks.
Project description:Pregnant C57Bl6N mice were treated with 0 (corn oil), 1.5, 3.0, or 6.0 ug/kg TCDD on gd14.5. Fetal hearts were collected on gd17.5. Hearts from each litter were pooled onto one chip. 4 replicates of each condition were run on affymetrix MG_U74Av2 chips, using standard affymetrix protocols and controls. Experiment Overall Design: 0 (corn oil), 1.5, 3.0, or 6.0 ug/kg TCDD, 4 replicates of each
Project description:The aryl hydrocarbon receptor (AHR) is a widely-expressed ligand-dependent transcription-factor that mediates cellular responses to dioxins and other planar aromatic hydrocarbons. Indeed, AHR-null mice are refractory to the physiological effects of dioxin-exposure. Although some mechanistic aspects of AHR activity are well understood, the tissue-specificity of AHR effects remains unclear, both during development and following administration of exogenous ligands. Previously we employed studied the transcriptional responses of wild-type and AHR-null C57BL/6J mice to dioxin-exposure. We found that essentially all hepatic effects of dioxin were mediated by the AHR, and that large numbers of genes were affected by dioxin exposure. Surprisingly, we also identified a large effect of AHR genotype, even in the absence of dioxin-exposure. To help assess the tissue-specificity of AHR activity we replicated that prior study in the kidney from the same animals previously studied, and extensively compared the hepatic and renal transcriptional profiles. We find that dioxin-exposure causes essentially no transcriptional effects in the absence of a functional AHR in either liver or kidney. Surprisingly, aside from a number of well-established AHR target genes, dioxin-exposure has few effects in animals harbouring a wild-type AHR. By contrast, AHR genotype profoundly remodels the renal transcriptome, and is associated with perturbation of specific functional pathways and with specific DNA motifs. Our results demonstrate the importance of inter-tissue comparisons and highlight the basal role of AHR activity in renal and hepatic development or normal physiology. Two-Factor, Two-Level. AHRnull and wildtype mice were treated with dioxin (TCDD) or corn oil vehicle. 3 replicates per treatment for AHRnull mice, 6 replicates of dioxin treatment for wildtype mice, and 5 replicates of corn oil treatment for wildtype mice.
Project description:Females were ovariectomized and injected with sesame oil, estradiol in sesame oil, BPA in sesame oil or HPTE in sesame oil. Uterine tissue was collected after 2 or 24 hours. RNA was analyzed by microarray compare ealry and late responses to a potent and a weak estrogen agaonist. 3 uteri per group were analyzed individually on one-color Agilent arrays (note: estradiol treatment at 24 hr only has 2 replicates).