Project description:The phosphorylomics data of liver tissue of 16-week-old HFHC-induced mice treated with saline or breviscapine for 8 weeks. The mice fed with high fat and high cholesterol were also divided into two groups. The control group was treated with normal saline for 8W, and the drug group was treated with breviscapine for 8W n=3.
Project description:The present study aimed to examine the effect of high-fat diet prior to pregnancy on the liver of mouse offspring. Female C57BL/6J mice were fed a normal chow (15.2% fat by energy) (CTR and CTR-PP groups) or a high-fat chow (31.2% fat by energy) (HFD and HFD-PP groups) for 3−4 weeks and then mated with male C57BL/6J mice fed normal chow. Some mothers continued on the same diet until pups reached 21 days of age (CTR and HFD), and others were fed the different chows from gestational day 0 (CTR-PP and HFD-PP) to determine the effects of a high-fat diet during the pre-pregnancy period in HFD-PP/CTR and HFD/CTR-PP comparisons. RNA sample was taken from liver of 3-week-old mouse prenatally received high-fat diet prior to pregnancy, during pregnancy and lactation, or through prior to and during pregnancy and lactation, while control RNA was taken from control counterpart prenatally received normal diet alone. Comparisons among groups were made by one-color method with normalized data from Cy3 channels for data analysis.
Project description:High fat diets are known to be a risk factor for prostate cancer. In this study, we investigated the effect of high fat diet on mouse prostate gene expression. C57BL/6J mice were fed either a control or high fat diet for 12 weeks. Microarray analyses were performed on mouse ventral prostate (VP) and dorsolateral prostate (DLP), followed by canonical pathway analysis and regulatory network identification. mRNA changes were confirmed by real time PCR. Approximately 2,125, and 1,194 genes responded significantly to the high fat diet in VP, DLP, respectively. Pathways and networks related to oxidative stress, glutathione metabolism, NRF-mediated oxidative stress response and NF-kappaB were all differentially regulated by high fat diet. GPx3 mRNA levels were decreased by approximately 2-fold by high fat diet in all 3 prostate lobes. In human non-transformed prostate cells (PrSC, PrEC and BPH-1), cholesterol loading decreased GPx3 expression, and increased H2O2 levels of culture medium. Troglitazone increased GPx3 expression in 3 normal prostate cells, and decreased H2O2 levels. In addition, troglitazone attenuated cholesterol-induced H2O2 increase. Tissue from prostate cancer biopsies had decreased GPx3 mRNA and its level was inversely related to the Gleason score. High fat diet alters pathways related to many genes concerned with oxidative stress. GPx3, a gene identified by this analysis, was found to be down regulated by high fat diet and appears be decreased in human prostate cancers, suggesting that GPx3 may have a possible role in modulating carcinogenesis. Control group:5 C57BL/6J mice (Taconic, Hudson, NY), 8-weeks of age, fed control diet ad libitum for 12 weeks; Experimental group: 5 C57BL/6J mice (Taconic, Hudson, NY), 8-weeks of age, fed ad libitum high fat diet for 12 weeks.
Project description:Time-course analysis of adipocyte gene expression profiles response to high fat diet. The hypothesis tested in the present study was that in diet-induced obesity, early activation of TLR-mediated inflammatory signaling cascades by CD antigen genes, leads to increased expression of pro-inflammatory cytokines and chemokines, resulting in chronic low-grade inflammation. Early changes in collagen genes may trigger the accumulation of ECM components, promoting fibrosis in the later stages of diet-induced obesity. New therapeutic approaches targeting visceral adipose tissue genes altered early by HFD feeding may help ameliorate the deleterious effects of a diet-induced obesity. Total RNA obtained from isolated epididymal and mesenteric adipose tissue of C57BL/6J mice fed normal diet or high fat diet for 2, 4, 8, 20 and 24weeks
Project description:The aim of this study was to evaluate the effects of olive oil phenols on brain aging in mice, focusing on changes in the microRNA profile. A sister experiment focusing on gene expression changes is also submitted to ArrayExpress under accession number E-MTAB-1530 ( http://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-1530/ )
Project description:A non-optimal fetal environment is known to cause low birth weight, which has been epidemiologically associated with a greater risk of adult diseases. Maternal undernutrition in animal models has also revealed the increased risks for adult diseases in the offspring. In this study, pregnant mice underwent overnight food deprivation at gestation day (GD)17 or 50% food restriction (FR) from GD10 to GD17, and the fetal brains were examined for global changes in gene expression by DNA microarray analysis utilizing the dye-swap approach. We present here a list of candidate genes from the fetal brain that might be responsible for developmental origins of health and disease. For food deprivation (FD), the pregnant mice were deprived of the food for overnight before lights were turned off on GD17. For food restriction (FR), pregnant mice were exposed to 50% food restriction (FR) from GD 10 to 17 and caesarean section was performed between 10:00-12:00 AM on GD18. Amount of CE-2 chow supplied to FR group was calculated as 50% of CE-2 consumed by control group each gestation day. Control group was supplied with chow ad libitum. Pregnant mice were sacrificed by cervical dislocation, and the fetuses were taken out and anesthetized on ice cold phosphate-buffered saline. The fetuses were dissected under a dissection microscope, and fetal tissues are carefully removed avoiding any other tissues contamination. The brain was collected from control (n=5) and FD (n=5) or FR (n=5) fetuses, and immediately frozen by immersion in liquid nitrogen. For DNA microarray analyses, the total RNA was extracted, quality and quantity determined, and total RNA from each sample (control and treatment) in each group was pooled, followed by established protocols for genome wide expression changes for both FD and FR samples using a 60-mer probes (4 x 44K (41,090 gene probes), mouse whole genome, Agilent) DNA chip by the dye-swap approach.
Project description:Breast cancer is one of leading causes of death worldwide in the female population. Deaths from breast cancer could be reduced significantly through earlier and more efficient detection of the disease. Saliva, an oral fluid that contains an abundance of protein biomarkers, has been recognized as a promising diagnostic biofluid that is easy to isolate through non-invasive techniques. Assays on saliva can be performed rapidly and are cost-effective. Therefore, our work aimed to identify salivary biomarkers present in the initial stages of breast cancer, where cell alterations are not yet detectable by histopathological analysis. Using state-of-the-art techniques, we employed a transgenic mouse model of mammary cancer to identify molecular changes in precancerous stage breast cancer through protein analysis in saliva. Through corroborative molecular approaches, we established that proteins related to metabolic changes, inflammatory process and cell matrix degradation are detected in saliva at the onset of tumor development. Our work demonstrated that salivary protein profiles can be used to identify cellular changes associated with precancerous stage breast cancer through non-invasive means even prior to biopsy-evident disease.
Project description:The main cause of morbidity and mortality in diabetes mellitus (DM) are cardiovascular complications. Diabetic cardiomyopathy (DCM) remains incompletely understood. Animal models have been crucial in exploring DCM pathophysiology while identifying potential therapeutic targets. Streptozotocin (STZ) has been widely used to produce experimental models of both type 1 and type 2 DM (T1DM and T2DM). Here we compared these two models for their effects on cardiac structure, function, and transcriptome. Different doses of STZ and different diet chows were used to generate T1DM and T2DM in C57BL/6J mice. Normal euglycemic and non-obese sex and age-matched mice served as controls (CTRL). Immunohistochemistry, RT-PCR, and RNA-Seq were employed to compare hearts from the three animal groups. STZ-induced T1DM and T2DM differently affect left ventricular function and myocardial performance. T1DM displays an exaggerated apoptotic cardiomyocyte (CM) death and reactive hypertrophy and fibrosis along with increased cardiac oxidative stress, CM DNA damage and senescence when compared to T2DM mice. T1DM and T2DM differently affect whole cardiac transcriptome. In conclusion, STZ-induced T1DM and T2DM mouse models show significant differences in cardiac remodeling, function and whole transcriptome. These differences could be of key relevance when choosing an animal model to study specific features of DCM.