Muscle expression of SOD1G93A modulates microRNA and mRNA expression pattern associated with the myelination process in the spinal cord of transgenic mice.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Camilla Bernardini
PROVIDER: E-GEOD-71194 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Expression profiling of lumbar spinal cord from MLC/SOD1G93A mice and age matched controls at 120 days of age. We used Affymetrix GeneChip Mouse Gene expression 2.0 st Array to determine differential gene expression. Samples were collected from mice MLC/SOD1G93A and controls FVB age matched at 4 month-old. Samples were collected representing each genotype and age group for RNA extraction and hybridization on Affymetrix Microarrays.
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Project description:Albeit increased serum CK level and abnormal muscle histology are always present, boys with DMD are phenotipically indistinguishable from the normal ones at birth and, in their first years of life, acquire early motor milestones at normal times. A clear defect in muscle function becomes generally apparent by the end of the second year. As the disease is typically diagnosed between the ages of 3 and 7, the first two years are often considered and referred to as clinically presymptomatic. As a defined gene expression signature was shown to characterize these symptomatic patients we sought to investigate whether and to which extent alterations may be also present in muscle from presymptomatic DMD infants. To this aim, we used the Affymetrix technology to compare the individual expression profiles of 19 DMD patients with age at biopsy scattered along the first two years of the disease with those of 14 age matched controls. This approach allowed us to describe with high resolution the altered transcriptional state that characterizes this early, presymptomatic phase of the disease and highlight some molecular pathways as potential critical targets in the pathophysiology of the disease. Experiment Overall Design: -Subjects Experiment Overall Design: Relevant data about the participants are posted under supplementary material (Table ST1). All DMD patients (n=22) had diagnosis of Duchenne Muscular Dystrophy based on the absence of dystrophin immunoreactivity on quadriceps muscle sections. None of the participants at the time of biopsy was or had been under corticosteroid treatment. Control biopsies (n=14) were selected from diagnostic specimens which were not given a diagnosis of neuromuscular disease nor showed any non-specific myopathic signs. A MIAME compliant description of this study is posted under supplementary Material (MIAME compliance). Experiment Overall Design: -RNA extraction. Experiment Overall Design: Total RNA was extracted from frozen quadriceps muscle biopsies by TriZol. (TriZol reagent, Invitrogen). RNA was further purified using the RNAeasy mini kit following the RNA cleanup protocol as indicated by the manufacturer (QIAGEN). RNA purity and integrity was assessed by spectophotometric analysis and agarose gel electrophoresis. Experiment Overall Design: -Affymetrix Genechips. Experiment Overall Design: In this work we made use of one chip type: the affymetrix HG-U133A genechipCRNA synthesis was performed using 5ug of total RNA as template, as described in the Affymetrix Gene Expression Manual. Genechips were washed and stained in an Affymetrix fluidic station 430. To avoid overcorrelation, samples were processed 8 at the time and arranged to have both DMD and control samples in each experimental session.
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Project description:Objective: identify novel and relevant aspects of Sorafenib action on liver cancer cells. We found that in rat hepatocholangiocarcinoma (LCSC-2) cells, exposure to the MEK/multikinase inhibitor sorafenib did not inhibit ERK phosphorylation nor induced appreciable cell death in the low micromolar range; instead, the drug elicited a raise of intracellular reactive oxygen species (ROS) accompanied by a severe decrease of oxygen consumption and intracellular ATP levels, all changes consistent with mitochondrial damage. Moreover, Sorafenib induced depolarization of isolated rat liver mitochondria, indicating a possible direct effect on the organelle. Microarray analysis of gene expression in sorafenib-trated cells revealed a metabolic reprogramming toward aerobic glycolysis, that likely accounts for resitance to drug toxicity in this cell line. Importantly, cytotoxicity was strongly potentiated by glucose withdrawal from the culture medium or by the glycolytic inhibitor 2-deoxy-glucose, a finding also confirmed in the highly malignant melanoma cell line B16F10. Mechanistic studies revealed that ROS are pivotal to cell killing by the Sorafenib + 2DG combination, and that a low content of intracellular oxidants is associated with resistance to the drug; instead, Thr172phosphorylation/activation of the AMP-activated protein kinase (AMPK), induced by Sorafenib, may exert protective effects, since cytotoxicity was enhanced by an AMPK specific inhibitor and prevented by the AMPK activator Metformin. Overall, this study identifies novel and relevant aspects of Sorafenib action on liver cancer cells, including mitochondrial damage, induction of ROS and a metabolic cell reprogramming towards “glucose addiction”, potentially exploitable in therapy. Microarray analysis of gene expression in sorafenib-trated cells. LCSC-2 cells were incubated with sorafenib 2.5 mM under serum deprivation for 12 hours. The total RNA was isolated from LCSC2, 24h after treatment, using the RNeasy mini kit (Qiagen, Hilden, Germany), RNA was quantified using a UV spectrophotometer and RNA quality and integrity were assessed Agilent 2100 Bioanalyzer (Agilent, Santa Clara, CA, USA). The resulting total RNA was then used to create the biotin-labeled library to be hybridized on GeneChip Rat Gene expression 1.0 st Array (Affymetrix, Santa Clara, CA, USA), according to the recommended experimental protocols provided by the suppliers. The CEL files resulting from the hybridization were analyzed using the Partek® Genomic Suite™ (Partek GS). Gene-level calculation was performed by Robust Multichip Average and normalization by quantile sketch.
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Project description:To predict Rp58-regulated gene involved in myogenesis, RNA profiling experiments were performed, comparing RNA derived from C2C12 with or without expressing shRNA for Rp58. As a result, 271 genes were upregulated in C2C12 stably expressing shRNA-Rp58 cells compared with control C2C12 cells. As Rp58 is repressor in C2C12, we hypothesized that Rp58 regulates gene cluster which expression is downregulated in accordance with Rp58 expression and myogenesis progression. In this regard, we also characterized dynamic gene expression patterns during myogenesis by microarray at 4 different stage (GM, day 0, 2, 4) of C2C12 myogenesis assays and found that 399 genes expression is characterized as downregulation pattern during myogenesis. Importantly, this down regulation gene set and upregulated genes by shRNA for Rp58 were highly overlapped. Experiment Overall Design: C2C12 murine skeletal muscle cells were purchased from American Type Experiment Overall Design: culture Collection (ATCC). These cells were mainteined in GM (DMEM Experiment Overall Design: supplemented with 10% FBS). Cells were grown in GM and after reaching Experiment Overall Design: counfluence, the medium was switched to DM (DMEM supplemented with 2% hourse serum) and further incubated. The medium was changed every 2 days. Culture was performed by using within five passages cells. For the experiment of shRNA for Rp58, transfection was performed by using Lipofectamin 2000 (Invitrogen). Stable transfectants were obtained by selection of the transfected C2C12 cells for two weeks. Experiment Overall Design: Microarray analysis - RNA was isolated as described from C2C12, and cRNA was synthesized. 10 ug of cRNA were hybridized to Affymetrix mouse 430 2.0 arrays. Intensity values were quantified using RMA algorithm. Experiment Overall Design: MAPPFinder (www.genmapp.org) was used to integrate expression data with known pathways.
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