ABSTRACT: Expression data from human primary skeletal muscle myotubes treated with aldosterone, spironolactone, eplerenone, mifepristone, prednisolone or vehicle
Project description:Expression data from human primary skeletal muscle myotubes treated with aldosterone alone or co-incubated with aldosterone plus spironolactone, eplerenone, or mifepristone
Project description:To test for a function effect of mineralocorticoid receptor modulation in skeletal muscle, global gene expression analysis was conducted on human myltubes treated with a mineralocorticoid receptor agonist or antagonist. 9 total samples were analyzed. 3 biological replicates for each of the following treatment groups were included: 1) aldosterone; 2) spironolactone; 3) vehicle (ethanol). Pairwise comparison between groups were carried out and a fold-change ≥2 were selected.
Project description:We report the RNA Sequencing of myleoid cells isolated from 4.5-week-old mdx mice that were administered spironolactone, prednisolone, or vehicle for 7 days. We find that both spironolactone and prednisolone downregulated expression of genes involved in inflammation and fibrosis, while prednisolone further perturbed cell cycle genes.
Project description:To identify the gene expression differences in skeletal muscles resulting from treatment of dystrophic mice with spironolactone plus lisinopril, eplerenone plus lisinopril or prednisolone.
Project description:The steroid hormone aldosterone plays a role in vascular function and disease. Aldosterone activates the mineralocorticoid receptor (MR), a ligand-activated transcription factor. MR have been found to be expressed in vascular cells and vessels. We used microarrays to identify the global programme of gene expression changes in mouse aortas treated with vehicle (DMSO) or aldosterone. Wild type C57Bl6 male mice were treated with spironolactone (20 mg/kg/day, an MR antagonist) for 5 days by Sub-cutaneous pellet to suppress basal MR-mediated gene expression. Aortas were then harvested and treated ex vivo in organ culture with vehicle or 100 nM aldosterone for 2, 4, or 8 hours. Three aortas were pooled for each timepoint and treatment, and three pooled biological replicates were performed.
Project description:The purpose of this study was to examine the effect of aldosterone receptor blockade on the immunopathogenesis and progression of nephritis in the (NZBxNZW) F1 murine lupus model. Female NZB/W F1 mice (11 weeks old) were treated daily with 25 or 50 mg/kg of oral spironolactone or vehicle. Proteinuria, renal function and serum autoantibody levels were monitored. Renal histopathology, immune complex deposition, and immunohistochemistry were analyzed at various time points. Targeted microarray analysis was performed on renal tissue, with subsequent real time PCR analysis of several differentially expressed genes. At 36 weeks of age, 8 mice from each treatment group (vehicle, 25 mg/kg/d spironolactone and 50 mg/kg/d spironolactone) were anesthetized and perfused with cold saline; then one kidney per mouse was removed , homogenized in Tripure, and frozen at -80 until RNA extraction. RNA was extracted using Tripure and a Qiagen RNEasy Minikit. RNA was pooled equally by weight within each treatment group and frozen at -80. Subsequently, the three batches of pooled RNA were processed for microarray analysis.
Project description:We identified the target genes of FTO ("fat mass and obesity associated") in primary cultures of human skeletal muscle cells using adenoviral vectors expressing FTO or GFP and oligonucleotide microarrays. Human myotubes were prepared from 4 different skeletal muscle biopsies. After differentiation, myotubes were infected for 48 hours with recombinant adenovirus expressing either GFP or FTO. Each FTO-infected myotubes culture was compared to GFP-infected myotubes culture. GFP-infected myotubes were regarded as the control. Four biological replicates were processed.
Project description:In this study we have identified the target genes of BHLHB2 and BHLHB3 in primary cultures of human skeletal muscle cells using adenoviral vectors expressing either BHLHB2 or BHLHB3, and oligonucleotide microarrays. Human myotubes were prepared from 4 different skeletal muscle biopsies. After 7 days of differentiation, myotubes were infected for 48 hours with recombinant adenovirus expressing either GFP, BHLHB2 or BHLHB3. Each BHLHB2- or BHLHB3-infected myotubes culture was compared to GFP-infected myotubes culture. GFP-infected myotubes were considered the control. Four biological replicates were processed.
