We propose comparing liver gene expression of WT and female ERKO mice early in the high-fat feeding period to animals fed a regular chow diet. Analyzing liver tissue before the fatty liver disease phenotype becomes severe will allow identification of target genes which may be causal.
Hormone signaling and fatty liver in females: analysis of estrogen receptor α mutant mice.
Sex, Specimen part
View SamplesThere are a few markers for embryonic hepatic stellate cells in mouse embryonic livers
Isolation of a unique hepatic stellate cell population expressing integrin α8 from embryonic mouse livers.
Specimen part
View SamplesThe glomerular filtration barrier prevents large serum proteins from being lost into the urine. It is not known, however, why the filter does not routinely clog with large proteins that enter the glomerular basement membrane (GBM). Here we provide evidence that an active transport mechanism exists to remove immunoglobulins that accumulate at the filtration barrier. We found that FcRn, an IgG and albumin transport receptor, is expressed in podocytes and functions to internalize IgG from the GBM. Mice lacking FcRn accumulated IgG in the GBM as they aged and tracer studies showed delayed clearance of IgG from the kidneys of FcRn deficient mice. Supporting a role for this pathway in disease, saturating the clearance mechanism potentiated the pathogenicity of nephrotoxic sera. These studies support the idea that podocytes play an active role in removing proteins from the GBM and suggest that genetic or acquired impairment of the clearance machinery is likely to be a common mechanism promoting glomerular diseases.
Podocytes use FcRn to clear IgG from the glomerular basement membrane.
Specimen part
View SamplesMajor causes of lipid accumulation in liver are increased import, synthesis or decreased catabolism of fatty acids. The latter is caused by dysfunction of cellular organelle controlling energy homeostasis, i.e. mitochondria. However, peroxisomes appear to be an important organelle in lipid metabolism of hepatocytes, but little is known about their role in the development of non-alcoholic fatty liver disease (NAFLD). To investigate the role of peroxisomes next to mitochondria in excessive hepatic lipid accumulation we used the leptin resistant db/db mice on C57BLKS background, a mouse model that develops hyperphagia induced diabetes with obesity and NAFLD.
Peroxisomes compensate hepatic lipid overflow in mice with fatty liver.
Sex, Age, Specimen part
View SamplesZebrafish of two different age groups (12 and 36 months) were treated with low amounts of rotenone (mild stress) and compared to untreated zebrafish. Two different durations were used (3 and 8 weeks). Illumina sequencing (HiSeq2000) was applied to generate 50bp single-end reads. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de) Overall design: 68 sample: 3 tissues (brain, liver, skin); 2 age groups (12 and 36 months); controls and rotenone treated samples; 2-6 biological replicates for each group
Longitudinal RNA-Seq Analysis of Vertebrate Aging Identifies Mitochondrial Complex I as a Small-Molecule-Sensitive Modifier of Lifespan.
No sample metadata fields
View SamplesGenetically targeted mice with deficiency for the A2BAR show increased susceptibility to acute myocardial ischemia and are not protected by IP, a powerful strategy for cardioprotection, where short and repeated episodes of ischemia and reperfusion prior to myocardial infarction result in attenuation of infarct size.
Adora2b-elicited Per2 stabilization promotes a HIF-dependent metabolic switch crucial for myocardial adaptation to ischemia.
Sex, Age
View SamplesEpithelial tumor cells (E) underwent EMT in vivo in FVB/N mice generating mesenchymal tumors. Mesenchymal cell lines (M1-M4) were each derived from a different mouse. This study compares gene expression between these two different tumor types.
Immune-induced epithelial to mesenchymal transition in vivo generates breast cancer stem cells.
No sample metadata fields
View SamplesNaturally occurring CD25+CD4+ regulatory T cells (T reg cells) are currently intensively characterized because of their major importance in modulating host responses to tumors and infections, in preventing transplant rejection, and in inhibiting the development of autoimmunity and allergy. Originally, CD4+ T reg cells were identified exclusively by the constitutive expression of CD25, and many in vivo experiments have been performed using depleting antibodies directed against CD25. However, both the existence of CD25 T reg cells, especially within peripheral tissues, as well as the expression of CD25 on activated conventional T cells, which precludes discrimination between T reg cells and activated conventional T cells, limits the interpretation of data obtained by the use of anti-CD25 depleting antibodies. The most specific T reg cell marker currently known is the forkhead box transcription factor Foxp3, which has been shown to be expressed specifically in mouse CD4+ T reg cells and acts as a master switch in the regulation of their development and function. To address the question of the in vivo role of T reg cells in immunopathology, we have generated bacterial artificial chromosome (BAC)transgenic mice termed depletion of regulatory T cell (DEREG) mice, which express a diphtheria toxin receptor (DTR) enhanced GFP (eGFP) fusion protein under the control of the foxp3 locus, allowing both detection and inducible depletion of Foxp3+ T reg cells. The gene expression profile of both CD4+eGFP+FoxP3+ and CD4+eGFPnegFoxP3neg cells isolated from DEREG mice was here analyzed by micro array.
Immunostimulatory RNA blocks suppression by regulatory T cells.
Specimen part
View SamplesCD38, a multi-functional membrane receptor and enzyme, consumes NAD+ to generate products such as cyclic-ADP-ribose. CD38 knockout mice show elevated tissue and blood NAD+ level. Chronic feeding of high-fat, high-sucrose diet to wild type mice leads to exercise intolerance and reduced metabolic flexibility. Loss of CD38 by genetic mutation protects mice from diet-induced metabolic deficit. These animal model results suggest that elevation of tissue NAD+ through genetic ablation of CD38 can profoundly alter energy homeostasis in animals that are maintained on a calorically-excessive Western diet.
Genetic Ablation of CD38 Protects against Western Diet-Induced Exercise Intolerance and Metabolic Inflexibility.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
SIRT1 redistribution on chromatin promotes genomic stability but alters gene expression during aging.
Sex, Age
View Samples