Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of mouse after gonadectomy and treatment with estradiol, dihydrotestosterone or vehicle to compare gene expression in gastrocnemius

ABSTRACT: Treatment of gonadectomized mice with estradiol, dihydrotestosterone or vehicle to compare gene expression in gastrocnemius.

ORGANISM(S): Mus musculus

SUBMITTER: Klara Sjögren

PROVIDER: E-MEXP-2192 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Publications

Stimulation of both estrogen and androgen receptors maintains skeletal muscle mass in gonadectomized male mice but mainly via different pathways.

Svensson Johan J Movérare-Skrtic Sofia S Windahl Sara S Swanson Charlotte C Sjögren Klara K

Journal of molecular endocrinology 20100430 1

Testosterone is a major regulator of muscle mass. Little is known whether this is due to a direct stimulation of the androgen receptor (AR) or mediated by aromatization of testosterone to estradiol (E(2)), the ligand for the estrogen receptors (ERs), in peripheral tissues. In this study, we differentiated between the effects mediated by AR and ER by treating orchidectomized (orx) male mice for 5 weeks with E(2) or the non-aromatizable androgen dihydrotestosterone (DHT). Both E(2) and DHT increas ...[more]

PMID: 20435684

Similar Datasets

Project description:Uterine receptivity implies a dialogue between the hormonally primed maternal endometrium and the free-floating blastocyst. Endometrial stromal cells proliferate, avert apoptosis, and undergo decidualization in preparation for implantation; however, the molecular mechanisms that underlie differentiation into the decidual phenotype remain largely undefined. The Notch family of transmembrane receptors transduce extracellular signals responsible for cell survival, cell-to-cell communication, and trans-differentiation, all fundamental processes for decidualization and pregnancy. Using a murine artificial decidualization model, pharmacological inhibition of Notch signaling by gamma-secretase inhibition resulted in significantly decreased deciduoma. Furthermore, a progesterone receptor (PR)-Cre Notch1 bigenic (Notch1d/d) confirmed a Notch1-dependant hypomorphic decidual phenotype. Microarray and pathway analysis, following Notch1 ablation, demonstrated significantly altered signaling repertoire. Concomitantly, hierarchical clustering demonstrated Notch1-dependent differences in gene expression. Uteri deprived of Notch1 signaling demonstrated decreased cellular proliferation; namely, reduced proliferation-specific antigen, Ki67, altered p21, cdk6, and cyclinD activity, and increased apoptotic-profile, augmented cleaved caspase-3, Bad, and attenuated Bcl2. Demonstrated here, the pre-implantation uterus relies on Notch signaling to inhibit apoptosis of stromal fibroblasts and regulate cell cycle progression, which together promotes successful decidualization. In summary, Notch1 signaling modulates multiple signaling mechanisms crucial for decidualization and we provide greater perspective to the coordination of multiple signaling modalities required during decidualization RNA samples from 3-5 separate mice were extracted. All mRNA quantities were normalized against 18S gene expression. Gene expression levels were measured by real-time RT-PCR SYBR Green analysis using the ABI Prism 7700 Sequence Detector System according to manufacturer’s instructions (Applied Biosystems).

Project description:Acute respiratory distress syndrome (ARDS) carries about a 50 percent mortality and is frequently associated with an infection (sepsis). Life-support treatment with mechanical ventilation rescues many patients, although superimposed infection or multiple organ failure can result in death. The outcome of a patient developing sepsis highly depends on the degree of pre-existing inflammation prior to the infection. In this study, we describe each stage of the inflammation process using a transcriptional approach and an animal model. Femelle C57BL6/J mice received an intraveinous oleic acid injection to induce an acute lung injury. PBMC expression patterns have been analyzed using a 9900 cDNA mouse microarray (MUSV29K). Our gene-expression analysis revealed marked changes in the immune and inflammatory response metabolic pathways, notably lipid metabolism and transcription. The early pro-inflammatory stage (1H-1H30) is characterized by the release of immune response and activation of inflammatory mechanisms. Later (3H-4H), the immune cells migrate into inflamed tissues through interaction with vascular endothelial cells. Finally, at late stages of lung inflammation (18H-24H), metabolism is deeply disturbed. Highly expressed pro-inflammatory cytokines activate transcription of many genes as well as lipid metabolism. This global overview of critical events occuring during lung inflammation is essential to understand infectious pathologies such as sepsis where inflammation and infection are interwined. From now on, it becomes possible to isolate the impact of a pathogen at the transcriptional level from the global gene expression modifications resulting from the infection associated with the inflammation. Also, our work allowed to identify genes involved in the response to inflammation. Among those, several may be potential target for gene therapy. Wild-type femelle C57Bl/6J mice, 7 weeks old, were obtained from Charles River and housed in a specific pathogen-free animal facility. We studied 39 mice divided into 6 groups. Each group was identified according to the incubation time: 1H, 1H30, 3H, 4H, 18H and 24H. The 1H group was made up of 6 mice (2 physiological serum and 4 OA); the 1H30 group was made up of 8 mice (2 physiological serum and 6 OA); the 3H group was made up of 7 mice (2 physiological serum and 5 OA); the 4H group was made up of 6 mice (2 physiological serum and 4 OA); the 18H group was made up of 6 mice (2 physiological serum and 4 OA); the 24H group was made up of 6 mice (2 physiological serum and 4 OA). Several RNA samples have been hybridized on 2 filters consisting in technical replicates. Data normalized by quantile without adjustment on physiological serum linked on Series record.

Project description:Background MeCP2, methyl-CpG-binding protein 2, binds to methylated cytosines at CpG dinucleotides, as well as to unmethylated DNA, and affects chromatin condensation. MECP2 mutations in females lead to Rett syndrome, a neurological disorder characterized by developmental stagnation and regression, loss of purposeful hand use and speech, stereotypic hand movements, deceleration of brain growth, autonomic dysfunction and seizures. Most mutations occur de novo during spermatogenesis. Located at Xq28, MECP2 is subject to X inactivation, and affected females are mosaic. Rare hemizygous males suffer from a severe congenital encephalopathy. Methods To identify pathways mis-regulated by MeCP2 deficiency, microarray-based global gene expression studies were carried out on cerebellum of Mecp2 mutant mice. We compared transcript levels in mutant/wildtype male sibs of two different MeCP2-deficient mouse models at 2, 4 and 8 weeks of age. Increased transcript levels were evaluated by real-time quantitative RT-PCR. Chromatin immunoprecipitation assays were used to document in vivo MeCP2 binding to promoter regions of candidate target genes. Results In the mutants, several hundred genes showed altered expression levels. Twice as many were increased than decreased, and only 27 genes were differentially expressed at more than one time point. The number of misregulated genes was 30% lower in mice with an exon 3 deletion (Mecp2tm1.1Jae) than in mice with a larger deletion (Mecp2tm1.1Bird). Between the mutants, few misregulated genes overlapped at each time point. Real-time quantitative RT-PCR assays validated increased transcript levels for four genes: Irak1, interleukin-1 receptor-associated kinase 1; Fxyd1, phospholemman, associated with Na, K-ATPase; Reln, encoding reelin, an extracellular signaling molecule essential for neuronal lamination and synaptic plasticity; and Gtl2/Meg3, an imprinted maternally expressed non-translated RNA that serves as a host gene for C/D box snoRNAs and microRNAs. Chromatin immunoprecipitation assays documented in vivo MeCP2 binding to promoter regions of Fxyd1, Reln, and Gtl2. Conclusions Transcriptional profiling of cerebellum failed to detect significant global changes in Mecp2-mutant mice. Increased transcript levels of Irak1, Fxyd1, Reln, and Gtl2 may contribute to the neuronal dysfunction in MeCP2-deficient mice and individuals with Rett syndrome. Our data provide testable hypotheses for future studies of the regulatory or signaling pathways that these genes act on. A genetic modification design type is where an organism(s) has had genetic material removed, rearranged, mutagenized or added, such as knock out. Computed

Dataset Information

Transcription profiling of mouse after gonadectomy and treatment with estradiol, dihydrotestosterone or vehicle to compare gene expression in gastrocnemius

Publications

Stimulation of both estrogen and androgen receptors maintains skeletal muscle mass in gonadectomized male mice but mainly via different pathways.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure