Project description:The aim of this experiment is to identify novel gene candidates being regulated in Fra-2 overexpressing mice. Fra-2 over-expressing mice (Fra-2 TG) develop vascular remodeling and pulmonary fibrosis. Fra-2, as a trascription factor, is responsible for downstream target genes expression. Comparison of the mRNA expressed from WT and Fra-2 TG animals will help to identify Fra-2 target genes. The microarray analysis will be performed in mRNA isolated from lung homogenate. The lungs of the mice were extensively perfused. The right part was snap-froen and transfered to (-80°C). The total RNA was isolated and quantified.
Project description:The aim of this experiment is to identify novel gene candidates being regulated in Fra-2 overexpressing mice. Fra-2 over-expressing mice (Fra-2 TG) develop vascular remodeling and pulmonary fibrosis. Fra-2, as a trascription factor, is responsible for downstream target genes expression. Comparison of the mRNA expressed from WT and Fra-2 TG animals will help to identify Fra-2 target genes. The microarray analysis will be performed in mRNA isolated from lung homogenate. The lungs of the mice were extensively perfused. The right part was snap-froen and transfered to (-80°C). The total RNA was isolated and quantified. Comparison of transgenes vs. wild-types. Hybridization of samples from 4 wild-type and 4 transgene animals = 8 single-color hybridizations
Project description:We hypothesized that gene expression in lungs of Fra-1+/+ and Fra-1-/- mice are divergent thus contributing fibrosis. More specifically, Fra-1-/- mice are increased susceptible to fibrosis. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between Fra-1+/+ and Fra-1-/- mice at early time point.
Project description:Microarray analysis of Fra-2 tg female and male mice at 8 weeks of their disease development give an indication of possible differentially regulated genes. Wildtype mice serve as a healthy control.The mRNA was obtained from lung homogenate of the mice (n=4/group for all). There was no treatment applied, we investigate the baseline differences.
Project description:We hypothesized that gene expression in lungs of Fra-1+/+ and Fra-1-/- mice are divergent thus contributing fibrosis. More specifically, Fra-1-/- mice are increased susceptible to fibrosis. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between Fra-1+/+ and Fra-1-/- mice at early time point. This study utilizes microarray analysis to test these hypotheses. 5 days PBS and bleomycin treated lung samples from both Fra-1+/+ and Fra-1-/- mice were used. RNA was isolated and used for global gene expression profiling (Affymetrix MoGene 1.0ST v1 Array). The raw probe signal intensities were quantile normalized over all samples, summarized with the robust multi-array average (RMA) algorithm and log2 transformed with a median polish, using the Affymetrix Power Tools. We considered a transcript cluster (gene-level) to be reliably expressed in a sample if the Affymetrix implemented DABG (detection above ground) p-value was less than 0.05. We used local-pooled-error (LPE) estimates and robust statistical tests for evaluating significance of each gene's differential expression in a comparison.
Project description:Fra-2tg mice develop spontaneous lung fibrosis. We carried out this sequencing with tissue from young animals before they develop the tissue fibrosis, to explore the early gene expression changes that might contribute to the phenotype.
Project description:In order to analyze the global changes in gene expression resulting from loss of Fra signaling, we performed a microarray experiment comparing Drosophila embryos containing a loss of function fra[3] mutation to age matched wildtype embryos. RNA extracted from fra[3] mutant vs. wildtype embryos were hybridized to the Affymetrix GeneChip Drosophila Genome 2.0 .
Project description:The polarization and activation of macrophages are controlled synergistically by transcription factors such as NF-κB and AP-1 transcription factor members. Surprisingly, little is known about the role of the Fra proteins, both members of the AP-1 transcription factor family, in macrophage activity. To determine the full profile of Fra network, microarray RNA expression analysis using Agilent Technologies platform was performed in wild-type, Fra-1ΔMxCre or Fra-2ΔLysMCre macrophages.
Project description:In order to analyze the global changes in gene expression resulting from loss of Fra signaling, we performed a microarray experiment comparing Drosophila embryos containing a loss of function fra[3] mutation to age matched wildtype embryos. RNA extracted from fra[3] mutant vs. wildtype embryos were hybridized to the Affymetrix GeneChip Drosophila Genome 2.0 . We selected Drosophila embryos at stage 13, which marks the onset of Fra expression in the embryonic CNS and the early stages of commissural axon guidance in the ventral nerve cord. RNA was extracted from both fra[3] and wildtype embryos. Hybridization experiments were performed on Affymetrix Drosophila Genome 2.0 microarrays.