Sf9 induction with methoxyfenozide and methoprene
Ontology highlight
ABSTRACT:
ORGANISM(S): Spodoptera frugiperda
SUBMITTER: frederique hilliou
PROVIDER: E-GEOD-30937 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2012-12-13 | E-GEOD-32486 | biostudies-arrayexpress
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2011-04-05 | E-GEOD-16775 | biostudies-arrayexpress
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Project description:Sf9 induction with methoxyfenozide and methoprene
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Project description:Specificity of interaction between a microRNA (miRNA) and its targets crucially depends on the seed region located in its 5’-end. It is often implicitly considered that two miRNAs sharing the same biological activity should display similarity beyond the strict six nucleotide region that forms the seed, in order to form specific complexes with the same mRNA targets. We have found that expression of hsa-miR-147b and hsa-miR-210, though triggered by different stimuli (i.e. lipopolysaccharides and hypoxia, respectively), induce very similar cellular effects in term of proliferation, migration and apoptosis. Hsa-miR-147b only shares a “minimal” 6-nucleotides seed sequence with hsa-miR-210, but is identical with hsa-miR-147a over 20 nucleotides, except for one base located in the seed region. Phenotypic changes induced after heterologous expression of miR-147a strikingly differ from those induced by miR-147b or miR-210. In particular, miR-147a behaves as a potent inhibitor of cell proliferation and migration. These data fit well with the gene expression profiles observed for miR-147b and miR-210, which are very similar, and the gene expression profile of miR-147a, which is distinct from the two others. Bioinformatics analysis of all human miRNA sequences indicates multiple cases of miRNAs from distinct families exhibiting the same kind of similarity that would need to be further characterized in terms of putative functional redundancy. Besides, it implies that functional impact of some miRNAs can be masked by robust expression of miRNAs belonging to distinct families. To compare the set of transcripts targeted by hsa-miR-147a, hsa-miR-147b and hsa-miR-210, we overexpressed these miRNAs in human lung adenocarcinoma A549 cells by transfecting them with synthetic pre-miRNAs or a synthetic “negative” pre-miRNA as a control (miR-Neg). RNA samples were harvested at 48 hours post-transfection and 3 independent experiments were carried out. 48 hours post-transfection, 3 independent experiments were performed in dye-swap: hsa-miR-147a versus miR-Neg; hsa-miR-147b versus miR-Neg; hsa-miR-210 versus miR-Neg.
2012-08-20 | E-GEOD-33247 | biostudies-arrayexpress
Project description:During embryogenesis, the cardiac cell fate is acquired as early as gastrulation. There is compelling evidence that embryonic stem cells (ESC) can recapitulate early steps in cardiogenesis. Identification from human pluripotent stem cells of early cardiovascular cell progenitors, at the origin of the first cardiac lineage, would shed light on human normal and pathological cardiogenesis and would pave the way toward cell therapy for cardiac degenerative diseases. Here, we report the isolation, and a phenotypic characterisation of an early Oct-4+, SSEA-1+, Mesp1+ population of cardiovascular progenitors derived from human pluripotent stem cells. This multipotential progenitor features the capability to generate cardiomyocytes as well as smooth muscle and endothelial cells. We further bring a proof of concept that these progenitors can be used in cardiac regenerative medicine as allografted in infarcted non human primate myocardium, they differentiate in ventricular myocytes without any adverse effect. One RNA sample from HUESC-POU5F1 was compared in dye-swap to undifferentiated HUESC. Three distinct RNA samples from BMP2-induced SSEA1+ cells were compared in dye-swap to paired remaining SSEA1-. Reference samples correspond to undifferentiated HUESC and to SSEA1 negative cells, respectively. population respectivement.
2011-02-08 | E-GEOD-20230 | biostudies-arrayexpress
Project description:Recent studies have identified miR-210 among a set of hypoxia-regulated miRNAs, and shown the central regulatory role played by HIF to control transcription of this miRNA. Contradictory data exist concerning the regulation and roles of miR-210 during cancer progression. miR-210 appears at the same time over-expressed in some solid tumors (breast, pancreas, head and neck carcinomas, gliomas) while often deleted in ovarian carcinoma. It has been shown that depending on the tissue type or cellular model, miR-210 was indeed able to either promote entry into the cell cycle and to inhibit apoptosis or rather repress tumor initiation. We show here deregulation of several miRNAs in human lung cancer biopsies, including an over-expression of miR-210 which appears specific of late-stages of the tumor (>stage 2). MiR-210 function was then analyzed in the lung adenocarcinoma cell line A549. We found that miR-210 induced a delayed inhibition of proliferation associated with an induction of cell death. We also observed that mir-210 induces a loss of mitochondrial membrane potential and the apparition of an aberrant mitochondrial phenotype. mRNA expression profiling of cells overexpressing mir-210 revealed a specific signature characterized by an enrichment in mir-210 predicted targets among the downregulated transcripts (57 out of 243, p<10-12). Functional annotation of this set of mir-210-regulated transcripts, which includes several subunits of Electron Transport Chain (ETC) complex I and complex II revealed enrichment for terms such as 'cell death' and 'mitochondrial dysfunction'. Two of these ETC subunits, predicted to be targets of mir-210 by several bioinformatics prediction tools, were experimentally confirmed after cloning of their respective 3'UTR in a luciferase reporter vector. Finally, we provide experimental evidence indicating that these mitochondrial alterations could modulate HIF via a positive regulatory loop. Overall, our data strongly suggest that mir-210 could mediate two apparently opposite functions: i) apoptosis through targeting of specific mitochondrial components ii) a modulation of HIF through a positive regulatory loop. We propose that this dual behavior can explain the contradictory data regarding the impact of miR-210 during cancer progression. Refer to individual Series. This SuperSeries is composed of the following subset Series: GSE18692: MiRNA and lung cancer (INCA project) - 40 miRNAs microarrays GSE18694: MiRNA and lung cancer (INCA project) - 26 RNG25k microarrays GSE18695: MiRNA and lung cancer (INCA Project) - 66 RNG25k microarrays
2010-09-30 | E-GEOD-18805 | biostudies-arrayexpress
Project description:Covering denuded dermal surface after injury requires migration, proliferation and differentiation of skin keratinocytes. To clarify the major traits controlling these intermingled biological events, we surveyed the genomic modifications occurring during the course of a scratch closure of cultured human keratinocytes. Using a DNA microarray approach, we report the identification of 161 new markers of epidermal repair. Expression data, combined with functional analysis performed with specific inhibitors of ERK, p38[MAPK] and PI3 kinases, demonstrate that kinase pathways exert very selective functions by precisely controlling the expression of specific genes. Inhibition of the ERK pathway totally blocks the wound closure and inactivates many early transcription factors and EGF-type growth factors. P38[MAPK] inhibition only delays âhealingâ, probably in line with the control of genes involved in the propagation of injury-initiated signalling. In contrast, PI3 kinase inhibition accelerates the scratch closure and potentiates the scratch-dependent stimulation of three genes related to epithelial cell transformation, namely HAS3, HBEGF and Ets1. Our results define in vitro human keratinocyte wound closure as a reparation process resulting from a fine balance between positive signals controlled by ERK and p38[MAPK], and negative ones triggered off by PI3 kinase. The perturbation of any of these pathways might lead to dysfunction in the healing process, as those observed in pathological wounding phenotypes, such as hypertrophic scars or keloids. Keywords: Transcriptome of healing keratinocytes The DNA microarray analysis concerning the identification of the genes altered in response to cell scratching was performed on 3 independent experiments, derived from 3 distinct cell cultures. Results were generated after 2 independent microarray analyses, meaning that each time point was the result of 6 independent analyses. The data relative to the effect of U0126, SB203580 and LY294002 on the transcriptomal healing response were obtained from 2 independent experiments performed using 2 distinct cell cultures. Results were generated after 2 independent microarray analyses. The cDNA microarray contained 4.200 distinct cDNA probes. It has been previously described in Moreilhon et al (11). Gene selection was based on relevance to inflammation, infection, differentiation, ion transport, cell signaling, cell migration, proliferation etc⦠A large fraction of the probes also corresponded to transcripts encoding membrane proteins. The list of the 4.200 probes is available at http://www.microarray.fr/IPMC/cDNA_microarray5k.html, and the microarray is archived in GEO under reference GSE1853. The cDNA probes were PCR amplified from cDNA derived from Universal Human Reference RNA (Stratagene) by reverse transcription. Probes had the following properties: 1) they have a normalized length of 250 +/- 19 bp; 2) they have a normalized GC content of 52 +/- 8%; 3) they were specific for a unique human gene; and 4) they were controlled by DNA sequencing. PCR products were purified by using QIAquick 96 PCR Purification Kit (Qiagen), resuspended in 3SSC with an average spotting concentration of 200 ng/μl. Microarrays were printed with a SDDC-2 (Bio-Rad) on homemade aldehyde-coated glass microscope slides. Data presented into the present manuscript only refer to sequence-verified probes. Each PCR product was spotted four times on each slide (2 independent clusters of 2 spots spatially separated), to reduce positional bias of the fluorescence readout. The CyDye-labelled first-strand cDNAs were generated with the CyScribe First-Strand cDNA Labelling Kit (RPN 2600, Amersham Pharmacia Biotech), as described in Moreilhon et al, using ten micrograms of total RNA as template. Unincorporated CyDye-nucleotides were removed using the Nucleotide Removal Kit (Qiagen). Data Collection and Analysis : Data Collection : Microarrays were scanned either on GenePix4000B or on ScanArray5000 (Perkin Elmer). Both machines provided similar results (not shown). 16-bits TIF images were quantified with the corresponding softwares (GenePix Pro 5.0 program (Axon Instruments) for the GenePix, and Quantarray for the ScanArray). Intensities (either total or background values) were defined as average intensities for each spot. Negative controls (ânegâ) were spotted on each slide. They corresponded to non mammalian mRNA sequences with no significant identity with any human sequences. Such spots were used as controls. Data was normalized using a dye-swap method as described by Moreilhon et al.. We found that this method, while requiring duplication of experiments, improves the reproducibility of the quantification. Scratched (S) and non-scratched (NS) RNA samples were reverse transcribed in the presence of known amounts of the corresponding non mammalian âcontrolâ RNAs namely DmdNaC and DGNaC added at a respective S/NS ratio of 5, 0.2. Only experiments showing a good correlation between the experimental and true ratios for these controls were kept for analysis. Results are expressed as average ratios of intensities in âscratched cellsâ over intensities in ânon-scratched cellsâ. Data was then analyzed and/or visualized with MEV , or with the stand-alone program GeneANOVA, and the SAMâs Excel⢠plugin . Lists of genes significantly down and up-regulated under the different experimental conditions were selected by analysis of variance or using SAM. For the analysis of variance, signal was modelled as proposed by Kerr and Churchill (17) according to: yijkg = μ + Ai + Dj + Tk + Gg + (TG)kg + (AG)ig + (DG)jg + εijkg (1), where yijkg is the fluorescent intensity of array i and dye j representing treatment k and gene g. μ, Ai, Dj, Tk, and Gg are factors representing average signals among the whole experiment, one array, one dye, one treatment, or one gene, respectively. (TG)kg, (AG)ig, and (DG)jg are two-factor interactions between treatment and gene, array and gene (spot effects), dye and gene, respectively. εijkg represents a residual noise component, modelled as a Gaussian distribution with mean 0 and variance ϲ. (TG)kg denotes differences in expression for particular treatment and gene combinations that are not explained by the average effects on these treatments and genes. They represent the effects of interest, which were modelled using GeneANOVA. SAM analysis was performed as described in Tusher et al. (16). Ontologies attached to each gene were then used to classify altered genes according to main biological themes. Annotation of our probes was also accessible through MEDIANTE, our own microarray database which stores annotations derived from public databases. Additional statistical analyses, including principal component analysis (PCA) were performed with GeneANOVA.
2010-05-27 | E-GEOD-6820 | biostudies-arrayexpress