GPNMB Involved in Ischemic and Dilated Cardiac Diseases
Ontology highlight
ABSTRACT: A microarray-based screening was conducted in rat hearts 24 hours after myocardial infarction (MI) with the aim to discover yet unknown molecules that might have an impact on cardiac pathophysiology.
Project description:Parkinson’s disease (PD) is the second most common neurodegenerative disease worldwide and the first involving motor symptoms. Deep brain stimulation (DBS) neurosurgery treatment through electrodes implanted to the subthalamic nucleus (STN) improves dramatically the debilitating motor symptoms of the disease due to yet unknown molecular mechanisms. Affymetrix human junction prototype microarrays (HJAY) of blood leukocytes mRNA from PD patients prior to, and following DBS neurosurgery treatment on electrical stimulation were compared to these of age- and gender-matched healthy control volunteers. About 95% of all human genes undergo alternative splicing, and alternative splicing is involved in human diseases and specifically in neurodegenerative diseases. Thus, the goal of this study was to detect alternatively spliced genes in PD patients prior to, and following DBS and to predict the effect of these on the functional level of change at the transcript level (such as exon inclusion, intron retention and nonsense-mediated decay events). Understanding the role of alternative splicing in neurodegenerative diseases will open new avenues to future novel approaches for early detection and neuroprotective treatment enabled by the development of future genetic therapeutics targeted at specific modified splice variants. A total of 11 blood leukocytes mRNA samples were analyzed: four from Parkinson's Disease (PD) patients pre-DBS treatment, three from PD patients tested again post-DBS (while being on electrical stimulation), three from age- and gender-matching healthy control (HC) volunteers, and one PD sample pre-DBS sample was re-stained and rescanned .
Project description:we discovered that medulloblastomas that form in Ptch mice are composed of three different sibtypes depending on the cell of origin and tumor progression. The goal was to identify gene signature that can distinguish the three subtypes RNA from tumor tissues from the three subtypes were extracted by Trizol and hybridized on Affy St1.0 chips for analysis
Project description:17-AAG treatment of MCF-7 Microarray <br><br> Files containing additional statistical analysis and data for meta-probesets are available on the FTP site for the experiment, in E-MTAB-339.additional.zip
Project description:The PI3K/Akt signaling pathway impacts various aspects of CD8 T cell homeostasis, such as effect versus memory cell differentiation, during viral infection. We used microarrays to determine which downstream molecules were affected and what other signaling pathways were interconnected with the Akt pathway by constitutive activation of Akt in LCMV-infected CD8 T cells. Splenocytes from naive P14/WT or P14/Akt mice were stained with anti-CD8 and anti-Ly5.1, and CD8 T cells were sorted using a FACSAria II instrument. Purified Ly5.1+ CD8 T cells from P14/WT or P14/Akt mice were transferred into B6 mice, which were subsequently infected with LCMV Armstrong. At day 8 post infection, splenocytes were stained with anti-CD8, anti-Ly5.1, anti-KLRG1, and anti-CD127. Following staining, short-lived effector cells (SLECs) and memory precursor effector cells (MPECs) were sorted using the FACSAria II instrument; the purity of the sorted cells was >95%. A total of 5 samples were analyzed, including WT naive, WT SLEC, WT MPEC, Akt naive and Akt SLEC.
Project description:Keratinocyte growth factor (KGF, fibroblast growth factor-7) is a fibroblast-derived mitogen, which stimulates proliferation of epithelial cells. The expression of KGF by dermal fibroblasts is induced following injury and it promotes wound repair. However, the role of KGF in cutaneous carcinogenesis and cancer progression is not known. We have examined the role of KGF in progression of squamous cell carcinoma (SCC) of the skin. Gene expression profiling was performed of three cutaneous SCC cell lines treated with KGF (10 ng/ml) for 24 h, comparable untreated cells and of normal unterated epidermal keratinocytes to explore KGF-responce in SCC cells. Three cutanous SCC cell lines (established from two primary and one metastatic tumors) were cultured to 70% confluency, serum starved (0% FCS) for 16 h and treated with rKGF (10 ng/ml) for 24 h. Comparable cell cultures were left untreated with rKGF. Normal epidermal keratinocytes from two individuals were cultured in specified keratinocyte culture medium to 70% confluency. All cell cultures were processed for RNA extraction and Affymetrix whole transcript microarray gene expression analysis. Thus, the samples included three untreated cutaeous SCC cell lines (n=3), the same three cell lines treated with rKGF (n=3) and untreated epidermal keratinocytes from two individuals (n=2). Normal keratinocytes served as reference samples to untreated skin SCC cells.
Project description:Using array CGH and fiber-FISH, we found that several human T-ALL have tandem duplication of the MYB gene on one allele, we used microarray gene expression analysis to determine if increased MYB expression correlates with gene duplication Keywords: cell type comparison RNA from 17 T-ALL cell lines
Project description:We analyzed a role of histone deacetylases in alternative splicing regulation. Using human exon arrays we identified a list of 683 genes whose splicing changes after HDAC inhibition with sodium butyrate. 6 samples (3 nontreated controls and 3 sodium butyrate treated cells)
Project description:We analyzed a role of Brd2 protein in transcription and alternative splicing. 289 genes change alternative splicing after Brd2 knockdown and 1459 genes alter gene expression compared to cells treated with negative control siRNA. 6 samples (3 independent samples of cells treated with Brd2 siRNA, 3 samples of cells treated with negative control siRNA)
Project description:This is one of expressional parts of the study. These data were correlated to epigenetic changes and CG density of genes in analyzed cells. The whole study has a following summary: To elucidate possible roles of DNA methylation and chromatin marks in transcription, we performed epigenetic profiling of chromosome 19 in human bronchial epithelial cells (HBEC) and in the colorectal cancer cell line HCT116 as well as its counterpart with double knockout of DNMT1 and DNMT3B (HCT116-DKO). We found that H3K9me3 forms intragenic chromatin blocks along genes with low CpG density in the gene body. Analysis of H3K36me3 profiles indicated that this mark associates either with active genes with low CpG density and H3K9me3 in the gene body or with active genes with high CpG density and DNA hypermethylation in the gene body. In HCT116 cells with double knockout of DNMT1 and DNMT3B, transcription of genes with low CpG density in the gene body was highly elevated and associated with promoter DNA demethylation and rearrangement of H3K9me3 and H3K36me3 occupation. Our finding suggests that similar to DNA methylation, H3K9me3 may play a role in intragenic gene regulation. Further, we observed that a combination of low CpG density in gene bodies together with H3K9me3 and H3K36me3 marking is a specific epigenetic feature of zinc finger (ZNF) genes, which comprise 90% of all genes carrying both histone marks on chromosome 19. For high CpG density genes, transcription and H3K36me3 occupancy were not changed in condition of partial or intensive loss of DNA methylation in gene bodies in the HCT116-DKO cell line. siRNA experiments with SETD2 knockdown in both HBEC and HCT116-DKO cell lines failed to reduce DNA methylation in gene bodies under conditions of H3K36me3 depletion. Our study suggests that the H3K36me3 and DNA methylation marks in gene bodies are established independently from each other and points to similar functional roles of intragenic DNA methylation and intragenic H3K9me3 for CpG-rich and CpG-poor genes, respectively. To elucidate how a loss of DNA methylation affects a gene expression and epigenome we studied colon cancer cell line HCT116 and its derivative, HCT116 DNMT1-/- DNMT3b -/- (HCT116-DKO). According to previous studies HCT116-DKO is characterized by 95% of loss of DNA methylation. In HCT116 and HCT116-DKO cells, we profiled diverse epigenetic marks and gene expression. Further a crosstalk between epigenetic changes and transcriptional changes was analyzed. This is the expressional part of study.
Project description:Micro-array experiment was performed on URECs (Urine-derived Renal Epithelial Cells) from a patient carrying recessive NPHP1 mutation. URECs were treated either with 0.04% of DMSO or 2µM of Alprostadil for 24h.