This SuperSeries is composed of the SubSeries listed below.
Identification of tissue-specific transcriptional markers of caloric restriction in the mouse and their use to evaluate caloric restriction mimetics.
Sex, Specimen part
View SamplesThe effect of a short-term calorie restricted diet was evaluated in heart in seven strains of mice
Identification of tissue-specific transcriptional markers of caloric restriction in the mouse and their use to evaluate caloric restriction mimetics.
Sex, Specimen part
View SamplesThe effect of a short-term calorie restricted diet was evaluated in gastrocnemius muscle (GASTROC) in seven strains of mice
Identification of tissue-specific transcriptional markers of caloric restriction in the mouse and their use to evaluate caloric restriction mimetics.
Sex, Specimen part
View SamplesThe effect of a short-term calorie restricted diet was evaluated in epididymal white adipose tissue (WAT) in seven strains of mice
Identification of tissue-specific transcriptional markers of caloric restriction in the mouse and their use to evaluate caloric restriction mimetics.
Sex, Specimen part
View SamplesThe effect of a short-term calorie restricted diet was evaluated in cerebral cortex in seven strains of mice
Identification of tissue-specific transcriptional markers of caloric restriction in the mouse and their use to evaluate caloric restriction mimetics.
Sex, Specimen part
View SamplesCalcific aortic valvular disease (CAVD) is characterized by sclerosis of the aortic valve leaflets and recent clinical studies have linked several other risk factors to this disease, including male sex. In this study we examined potential sex-related differences in gene expression profiles between porcine male and female valvular interstitial cells (VICs) to explore possible differences in CAVD propensity on the cellular level.
Sex-related differences in gene expression by porcine aortic valvular interstitial cells.
Sex, Specimen part
View SamplesBackground & Aims: MiRNAs are small (~22 nucleotide), non-coding RNA molecules that regulate gene expression through imperfect complementarity with target messenger RNAs. The function of miRNA in mammalian organogenesis is largely unknown. Conditional loss-of-function of Dicer, the enzyme that processes precursor miRNA transcripts into their mature, active form, has been shown to cause severe defects in a number of organ systems. Here we address the role of Dicer in liver development and function. Methods: Mice lacking Dicer function in hepatocytes were generated using an Afp-Cre strain to drive deletion of a floxed Dicer allele. Deletion of the flox-dicer allele was confirmed by quantitative PCR. Decreased miRNA levels detected by quantitative RT-PCR and in situ hybridization confirmed loss of Dicer function. Gene expression microarray analysis was performed on liver RNA from P28 mutant and control mice. Liver sections from mutant and control mice ranging from embryonic stages through 3-4 months of age were examined and liver function tests were performed on adult mice. Results: Mice lacking hepatocyte Dicer function were born alive at the expected frequency, and had grossly normal appearance and behavior. Despite the loss of mature miRNA, hepatic function was normal, as reflected by normal blood gludose, albumin, cholesterol, and bilirubin. However, mutant mice between 2-4 months of age exhibit progressive hepatocyte damage, elevated ALT/AST, with evidence of balanced proliferation and apoptosis in the lobule. Microarray analysis indicates large-scale changes in gene expression, with increased expression of many miRNA targets, as well as imprinted genes. Conclusions: Loss of miRNA processing in the liver at late gestation has a remarkably mild phenotype, suggesting that miRNAs do not play an essential role in hepatic physiology. However, miRNA deficiency results in hepatocyte apoptosis and balanced hepatocyte regeneration. Finally, microarray analysis of gene expression in mutant liver suggests a previously unrecognized role for Dicer in the repression of imprinted genes.
Hepatic function is preserved in the absence of mature microRNAs.
Age, Specimen part
View SamplesThe goal was to identify genes targeted by miR-30a.
The microRNA-30 family is required for vertebrate hepatobiliary development.
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View SamplesAdult BALB/c female mice were injected intraperitoneally with a single dose at 20 mg per kg of antisense oligonucleotide either against miR-29a (5-TAACCGATTTCAGATGGTGCTA-3) or against a scrambled sequence (5-TCATTGGCATGTACCATGCAGCT-3 Antisense oligonucleotides contained 2-O-methoxyethyl (2-MOE), 2-flouro (2-F) 2'-alpha-flouro units with a phosphorothioate backbone (Regulus Therapeutics). Six days following the injection, liver was isolated, total RNA was prepared as described above, and the RNA was amplified and biotinylated using the MessageAmp Premier kit (Ambion). Samples (n=4 each experimental and control) were hybridized to Affymetrix GeneChip Mouse Genome 430 2.0 Arrays in the Childrens Hospital of Philadelphia Nucleic Acids Core Facilityand analyzed with the assistance of the Penn Bioinformatics Core. Probe intensities were normalized using the GCRMA method and the significance of the log2-transformed, GCRMA-normalized signal intensities was determined using SAM
MicroRNA profiling identifies miR-29 as a regulator of disease-associated pathways in experimental biliary atresia.
Sex, Specimen part, Treatment
View SamplesIn this study, we explored x-inactivation in monkey embryos (ICM and TE separately) and pluripotent stem cells (IVF derived ES, SCNT-derived ES and monkey iPS)
X-chromosome inactivation in monkey embryos and pluripotent stem cells.
Sex, Specimen part
View Samples