This study demonstrates that arthritis and heart valve stenosis comorbidity, the most common condition among RA and SpA patients, share common mesenchymal requirements converging in the pathogenic activation of resident mesenchymal origin fibroblasts in the Tnf?ARE mouse model. TNFR2 signaling, in this context, orchestrates the molecular mechanisms underlying arthritis and heart valve stenosis manifestation by regulating fibroblasts pathogenic activation status, cell proliferation and pro-inflammatory milieu. Finally this work highlights the complexity of TNFR2 functions since mesenchymal signaling is detrimental, whereas systemic TNFR2 provides protective signals that contain both pathologies Overall design: 3' RNA-Seq (QuantSeq) profiling of 2 cell types (SFs,VICs) in two different genotypes (TNF-DeltaARE, ColVIp75f/f-TNF-DeltaARE) and Wild type as control. 3 replicates per group.
Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.
Specimen part, Cell line, Subject
View SamplesObjective: Physical exercise and vitamin E are considered effective treatments of nonalcoholic fatty liver and other metabolic diseases. However, vitamin E has also been shown to interfere with the adaptation to exercise training, in particular for the skeletal muscle. Here, we studied the hypothesis that vitamin E also interferes with the metabolic adaptation of the liver to acute exercise.
A Vitamin E-Enriched Antioxidant Diet Interferes with the Acute Adaptation of the Liver to Physical Exercise in Mice.
Sex, Specimen part
View SamplesWhite adipose tissue is primary involved in the response to insulin after feeding, while brain is not directly sensitive to insulin levels.
eIF6 coordinates insulin sensitivity and lipid metabolism by coupling translation to transcription.
Specimen part
View SamplesLiver is primary involved in the response to insulin after feeding. Hepatocytes activates a tightly controlled genetic programme where specific sets of genes are modulates in response to insulin, for activation of the anabolic pathways.
eIF6 coordinates insulin sensitivity and lipid metabolism by coupling translation to transcription.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A history of obesity leaves an inflammatory fingerprint in liver and adipose tissue.
Sex, Age, Specimen part
View SamplesDieting is a popular yet often ineffective way to lower body weight, as the majority of people regain most of their pre-dieting weights in a relatively short time. The underlying molecular mechanisms driving weight regain and the increased risk for metabolic disease are still incompletely understood. Here we investigate the molecular alterations inherited from a history of obesity. In our model, male HFD fed obese C57BL/6J mice, were switched to a low caloric chow diet, resulting in a decline of body weight to that of lean mice. Within seven weeks after diet switch, most obesity associated phenotypes, such as body mass, glucose intolerance and blood metabolite levels were reversed. However, hepatic inflammation, hepatic steatosis as well as hypertrophy and inflammation of perigonadal, but not subcutaneous, adipocytes persisted in formerly obese mice. Transcriptional profiling of liver and perigonadal fat revealed an upregulation of pathways associated with immune function and cellularity. Thus, we show that weight reduction leaves signs of inflammation in liver and perigonadal fat, indicating that persisting proinflammatory signals in liver and adipose tissue could contribute to an increased risk of formerly obese subjects to develop the metabolic syndrome upon recurring weight gain.
A history of obesity leaves an inflammatory fingerprint in liver and adipose tissue.
Sex, Age, Specimen part
View SamplesGene expression profiles generated from skeletal muscle biopsies taken from participants of the HERITAGE family study. Participants completed an endurance training regime in which a skeletal muscle biopsy was taken prior to the start and after the final session of the program. Biopsies were used to generate Affymetrix gene expression microarrays.
The Role of Eif6 in Skeletal Muscle Homeostasis Revealed by Endurance Training Co-expression Networks.
No sample metadata fields
View SamplesWe performed gene expression microarray analysis of skeletal muscle biopsies from normal glucose tolerant subjects and type 2 diabetes subjects obtained during a 60 min bicycle ergometer exercise and the 180 min of recovery phase
Type 2 diabetes alters metabolic and transcriptional signatures of glucose and amino acid metabolism during exercise and recovery.
Age
View SamplesWe used microarrays to investigate differential gene expression in different thyroid hormone receptor beta mouse models. Hypothyroid wild type, TRbeta KO and TRbeta GS mutant mice were treated with T3 or vehicle alone. Microarray analysis revealed that the gene expression pattern in TRbeta GS mutant mice was similar to that in TRbeta KO mice.
Noncanonical thyroid hormone signaling mediates cardiometabolic effects in vivo.
No sample metadata fields
View SamplesIn this survey we effectively combined transcriptomics, proteomics and targeted-metabolomics to analyse the temporal relationship of alterations in liver preceding and accompanying the development of HFD-mediated hepatic insulin resistance. To assess HFD-mediated alterations in physiological parameters, insulin sensitivity, and molecular adaptations in liver male C3HeB/FeJ mice treated with a high-fat diet (HFD) for 7, 14, or 21 days and compared to age- matched controls fed low-fat diet (LFD).
High fat diet-induced modifications in membrane lipid and mitochondrial-membrane protein signatures precede the development of hepatic insulin resistance in mice.
Sex, Age, Treatment, Time
View Samples