Satellite cells are the primary source of stem cells for skeletal muscle growth and regeneration. Since adult stem cell maintenance involves a fine balance between intrinsic and extrinsic mechanisms, we performed genome-wide chronological expression profiling to identify the transcriptomic changes involved in acquisition of muscle stem cell characteristics.
Gene Expression Profiling of Muscle Stem Cells Identifies Novel Regulators of Postnatal Myogenesis.
Age, Specimen part
View SamplesDevelopment of Pectoralis major has been investigated through gene expression analysis in comparing animals receiving a restricted diet in P and Ca (NC), a normal diet with sufficient level of P and Ca (PC), and a restricted diet supplemented with phytase (Phy1000).
Exploratory transcriptomic analysis in muscle tissue of broilers fed a phytase-supplemented diet.
Specimen part
View SamplesWe recently isolated and identified (7E)-9-oxohexadec-7-enoic acid (1) and (10E)-9-oxohexadec-10-enoic acid (2) from the marine algae Chaetoceros karianus. Synthesis and biological characterization show that these are PPARa/? dual agonists. Herein we report the gene expression data from human SGBS pre-adipocytes, stimulated to differentiate with 1, 2 or the classical PPAR? agonist rosiglitazone. The transcriptome analysis shows that both compounds induce anti-diabetic gene programs in adipocytes by upregulating insulin-sensitizing adipokines and repressing pro-inflammatory cytokines. Overall design: Human SGBS pre-adipocytes were stimulated with adipogenic media supplemented with either (7E)-9-oxohexadec-7-enoic acid, (10E)-9-oxohexadec-10-enoic acid, or rosiglitazone from day 0 to day 4. On day 4, agonists were withdrawn, and the cells were allowed to differentiate following standard protocol. On day 8, RNA was isolated and sent to sequencing.
Synthesis and biological evaluations of marine oxohexadecenoic acids: PPARα/γ dual agonism and anti-diabetic target gene effects.
Specimen part, Cell line, Subject
View SamplesThe neurobiological functions of a number of kinases expressed in the brain are unknown. Here, we report new findings on DCLK3 (Doublecortin-like kinase 3) which is preferentially expressed in neurons in the striatum and dentate gyrus. Its function has never been investigated. DCLK3 expression is markedly reduced in Huntington''s disease. Recent data obtained in studies related to cancer suggest DCLK3 could have anti-apoptotic effect. Thus, we hypothesized that early loss of DCLK3 in Huntington''s disease may render striatal neurons more susceptible to mutant huntingtin (mHtt). We discovered that DCLK3 silencing in the striatum of mice exacerbated the toxicity of an N-terminal fragment of mHtt. Conversely, overexpression of DCLK3 reduced neurodegeneration produced by mHtt. DCLK3 also produced beneficial effects on motor symptoms in a knock-in mouse model of Huntington''s disease. Using different mutants of DCLK3, we found that the kinase activity of the protein plays a key role in neuroprotection. To investigate the potential mechanisms underlying DCLK3 effects, we studied the transcriptional changes produced by the kinase domain in human striatal neurons in culture. Results show that DCLK3 regulates in a kinase-dependent manner the expression of many genes involved in transcription regulation and nucleosome/chromatin remodeling. Consistent with this, histological evaluation showed DCLK3 is present in the nucleus of striatal neurons and, protein-protein interaction experiments suggested that the kinase domain interacts with zinc finger proteins, including TADA3, a core component of SAGA complex. Our novel findings suggest that the presence of DCLK3 in striatal neurons may play a key role in transcription regulation and chromatin remodeling in these brain cells, and show that reduced expression of the kinase in Huntington's disease could render the striatum highly vulnerable to neurodegeneration. Examination of DCLK3 as neuroprotector against mutant huntingtin in vivo and in vitro models. Overall design: Examination of DCLK3 as neuroprotector against mutant huntingtin in vitro experiments.
The striatal kinase DCLK3 produces neuroprotection against mutant huntingtin.
Specimen part, Cell line, Subject
View SamplesTwo human acute lymphoblastic leukemia cell lines (Molt-4 and CCRF-CEM) were treated with direct (A-769662) and indirect (AICAR) AMPK activators. Molt-4 and CCRF-CEM cells were obtained from ATCC (CRL-1582 and CCL-119). Control samples were used for the analysis of metabolic differences between cell lines. Therefore the data was analyzed in combination with, metabolomic data, and the genome-scale reconstruction of human metabolism. For experiments cells were grown in serum-free medium containing DMSO (0.67%) at a cell concentration of 5 x 105 cells/mL.
Prediction of intracellular metabolic states from extracellular metabolomic data.
Cell line, Treatment
View SamplesDifferentially expressed genes between 171 human soft tissue sarcomas with complex genomics
From PTEN loss of expression to RICTOR role in smooth muscle differentiation: complex involvement of the mTOR pathway in leiomyosarcomas and pleomorphic sarcomas.
Sex, Specimen part, Cell line
View SamplesMaddalena et al. showed that the limited DNA transfer capacity (~4.7kb) of adeno associated viral (AAV) vectors can be expanded up to 14kb with triple AAV vectors for the efficient expression of the therapeutic CDH23 (10.1kb) and ALMS1 (12.5kb) genes. Overall design: cells infected with triple AAV vectors carrying 2 different transgenes in 3 biological replicates; RNA extracted from WT cells was used as control .
Triple Vectors Expand AAV Transfer Capacity in the Retina.
Cell line, Subject
View SamplesOne of the main problems in managing desmoids tumors is their locoregional aggressiveness and their high ability to recur after initial treatment. In our work, with the goal to identify molecular markers that can predict Progression-Free Survival, gene-expression screening was conducted on 128 available independent untreated primary desmoid tumors using cDNA microarray. By analyzing expression profiles, we have identified, for the first time, a gene expression signature that is able to predict Progression-Free Survival. This molecular signature identified two groups with clearly distinct Progression-Free Survival in the two sets of subjects. Patients in good prognostic group had achieved a progression-free 2-year survival rate of 86% while patients in poor prognostic group had a progression-free 2-year survival rate of 44%.
Gene Expression Profiling of Desmoid Tumors by cDNA Microarrays and Correlation with Progression-Free Survival.
Sex, Age, Specimen part
View SamplesFor this study, we selected, from the French Sarcoma Group (FSG) database, soft tissue sarcomas with no recurrent chromosomal translocations and for which a frozen tissue of the untreated primary tumor was available. Three hundred and ten sarcomas have been studied. They are split in two cohorts.
Validated prediction of clinical outcome in sarcomas and multiple types of cancer on the basis of a gene expression signature related to genome complexity.
Specimen part, Disease, Time
View SamplesBatf3 regulates key CD8alpha DC-specific genes.
Compensatory dendritic cell development mediated by BATF-IRF interactions.
Specimen part
View Samples