Vagotomy-dependent stomach gene expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE30295 | GEO | 2014/09/02
SECONDARY ACCESSION(S): PRJNA143793
REPOSITORIES: GEO
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Project description:We have previously reported human gastrin overexpressing transgenic mice (=INS-GAS mice) and Helicobacter felis (=H.felis) infection synergistically accelerated gastric cancer in mice stomachs. (Wang et al 2000) Using this mouse model, we employed microarray analysis of gene expression profiling to identify gastric cancer-specific genes. Experiment Overall Design: 30 male INS-GAS mice (FVB/N background) were divided into groups: 15 mice were infected with H.felis at the age of 2-3 months and another 15 mice were not infected. 30 male non-transgenic FVB/N mice were also divided into 2 groups: 15 mice were infected with H.felis at the age of 2-3 months and another 15 mice were not infected. All mice were sacrificed after 6 months of H.felis infection, and total RNAs were extracted from whole stomachs. Experiment Overall Design: Histological analysis confirmed all of the stomachs in H.felis infected INS-GAS mice (=INSGAS+Hf) had intra-epithelial gastric cancer, and some of them also had invasion into submucosa, but none of them had distant metastatic lesions. Other 3 control groups had following histology in stomachs. (1) non-transgenic mice with H.felis infection (=FVB+Hf): severe intestinal metaplasia and/or mild dysplasia. (2) INS-GAS mice without infection (=INSGAS wt): severe atrophic gastritis and/or mild intestinal metaplasia (3) non-transgenic mice without infection (=FVB wt): normal stomach. Total RNAs extracted from each mouse in 4 different groups were used for microarray analysis of Affymetrix GeneChip. Experiment Overall Design: Up- or down-regulated genes in INSGAS+Hf group compared with all 3 control groups (FVB+HF, INSGAS wt and FVB wt) may represent gastric cancer-specific genes.
2008-06-13 | E-GEOD-4651 | biostudies-arrayexpress
Project description:We are now trying to elucidate the mechanism of Helicobacter-induced gastritis and gastric cancer. To identify genes involved in these Helicobacter-associated diseases, we infected Helicobacter felis to INS-GAS (insulin-gastrin transgenic) mice (C57BL/6 background) which shows accelerated development of gastritis and gastric cancer. Three infected mice and three uninfected control mice (6 in total) were sacrificed periodically (2, 4, 6, 8 months after the infection), and total RNA was isolated from each stomach. These samples are subjected to gene microarray analysis. Samples were obtained from mouse stomachs at 2, 4, 6, and 8/9 month post infection intervals. Control time points were taken at 0, 2, 4, 6, and 8 months. All samples, 22 in total, were hybridized to the GLYCOv2 array.
2011-02-17 | E-GEOD-27361 | biostudies-arrayexpress
Project description:The leptomeninges envelop the central nervous system and contribute to brain homeostasis by producing trophic factors and regulating entrance of cells, factors and agents, immune responses and cerebrospinal fluid production. We report that leptomeninges from adult mice are regionally patterned. Leptomeninges dissected from anterior or posterior aspects of the forebrain grown in hetero- or homo-typic culture with anterior and posterior cortical cells demonstrate differences in ability to support survival of neuronal subsets and proliferation of progenitors for astrocytes and oligodendrocytes. Meningeal support changes with age: co-culture with 18-month old leptomeninges reduced numbers of cortical progenitor cells and neurons but increased astrocyte expansion. Analysis of cytokine secretion and single cell RNA-sequencing revealed differences in anterior versus posterior, young versus old meningeal factors and composition. These data demonstrate that adult leptomeninges are regionally patterned in cell composition and functional properties, and suggest that meningeal deficits may contribute to brain aging and disease.
2021-11-01 | GSE139922 | GEO
Project description:The in vivo function of AGR2 was examined by generating an AGR2 null mouse. The mice died prematurely due to hyperplasia and dysplasia of the glandular stomach. Gene expression profiling was performed to compare differences in transcription between wild-type and null AGR2 mice. Female AGR2 wild-type and knockout mice were sacrificed at the age of 26 weeks and the glandular stomachs were removed. Total RNA was isolated using TRIzol reagent (Invitrogen, Carlsbad, CA). The RNA was was reverse transcribed, labeled, and hybridized to mouse oligonucleotide DNA microarrays (Illumina MouseRef-8 v2 Expression BeadChip)
2012-12-01 | E-GEOD-40062 | biostudies-arrayexpress
Project description:Actinomyces oralis strain:stomach | isolate:stomach Genome sequencing
| PRJNA708187 | ENA
Project description:Purpose: Despite demonstrating that the overall effect of long-term rapamycin-treatment is overwhelmingly positive in aging skeletal muscle, we observed muscle-specificity in the responsiveness to rapamycin, leading us to hypothesize that the primary drivers of age-related muscle loss and therefore effective intervention strategies may differ between muscles. To address this question and dissect the key signaling nodes associated with mTORC1-driven muscle aging, we created a comprehensive multi-muscle gene expression atlas in adult, sarcopenic and rapamycin-treated mice using RNA-seq. Methods: To examine the impact of long-term rapamycin treatment, male C57BL/6 mice were fed encapsulated rapamycin incorporated into a standardized AIN93M diet at 42 ppm (i.e. mg per kg of food), corresponding to a dose of ~4 mg·kg-1·day-1, from 15- to 30-months of age. This dose of rapamycin has been shown to extend lifespan maximally in male C57BL/6 mice. We performed RNA-seq on gastrocnemius (GAS), tibialis anterior (TA), triceps brachii (TRI) and soleus (SOL) muscles from each of six mice for 10m, 30m and 30mRM groups. The four muscle types were chosen to encompass fore- and hindlimb locations (e.g. TRI and GAS); slow and fast contraction properties (e.g. SOL and GAS); anterior and posterior positioning (e.g. TA and GAS) and the extent of protection by rapamycin (TA and TRI: protected; SOL: partiallly protected; GAS: not protected). Results: Age-related gene expression changes were remarkably consistent across the four different muscles, varying only in magnitude. Despite having the smallest age-related muscle loss of the four muscles, TA had the strongest age-related gene expression response which was associated with an increased reinnervation response. Despite the strong between-muscle commonality of age-related changes, gene expression responses to prolonged rapamycin treatment differed substantially between muscles. Rapamycin partially reversed many age-related changes in mRNA expression in the TA and TRI, but not in SOL or GAS muscle. Principle component analysis (PCA) showed that rapamycin had common 'anti-aging' effects on all muscles, while also exerting muscle-specific pro-aging effects on muscles not protected by rapamycin. Conclusions: Sustained, muscle fiber-specific mTORC1 activity drives sarcopenia-like gene expression programs, and the hyperactive mTORC1 seen in sarcopenic muscle may therefore contribute to sarcopenia.
2020-06-19 | GSE139204 | GEO