Newcastle disease virus (NDV) is an avian virus that selectively replicates and kills many different types of cancer cells and is being developed for cancer treatment. Our aim was to establish persistent infection in EJ28 and TCCSUP bladder cancer cells and identify the dysregulated genes and disrupted molecular pathways associated with persistent infection.
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Sex, Age, Specimen part, Disease, Cell line
View SamplesThe RNA-Seq experiment was performed to test whether loss of CHD7 does not affect the expression of DNA double-strand break repair proteins.
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Sex, Specimen part, Cell line, Treatment
View SamplesNo description.
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Sex, Specimen part, Treatment
View SamplesCardiovascular disease remains the number one global cause of death and presents as multiple phenotypes in which the interplay between cardiomyocytes and cardiac fibroblasts (CFs) has become increasingly highlighted. Fetal and adult CFs influence neighboring cardiomyocytes in different ways. Thus far, a detailed comparison between the two is lacking. Using a genome-wide approach, we identified and validated 2 crucial players for maintaining the adult primary human CF phenotype. Knockdown of these factors induced significant phenotypical changes, including senescence and reduced collagen gene expression. These may now represent novel therapeutic targets against deleterious functions of CFs in adult cardiovascular disease.
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View SamplesBackground and aims: Despite proven clinical efficacy of vedolizumab (VDZ) for inducing and maintaining remission in patients with Crohn's disease (CD) and ulcerative colitis (UC), subgroups of patients have no therapeutic benefit from anti-a4ß7 integrin therapy with VDZ. Within this study, we aimed to identify genetic, cellular and immunological mechanisms that define response and failure to VDZ treatment.Methods: Intestinal RNA Sequencing was performed in UC and CD patients before and at week 14 of VDZ therapy. a4ß7 expression on peripheral and mucosal immune cells was assessed by flow cytometry and immunohistochemistry. Cellular modes of VDZ mediated action were analysed ex vivo and in VDZ treated IBD patients.Results: Transcriptome analysis showed an impairment of signaling cascades associated with adhesion, diapedesis and migration of granulocytes and agranulocytes upon VDZ therapy. In non-remitters to VDZ therapy, a tissue destructive and leucocyte mediated inflammatory activity with activation of TNF dependent pathways was present, all of which were inhibited in remitters to VDZ. Clinical remission was associated with a significant reduction of a4ß7 expression on Th2 and Th17 polarized mucosal CD4+ T cells at week 14 of VDZ therapy and with significantly higher numbers of a4ß7 expressing mucosal cells prior to the initiation of VDZ therapy compared to non-remitters.Conclusions: Intestinal a4ß7 expression prior to VDZ therapy might represent a biomarker that predicts therapeutic response to subsequent VDZ treatment. Due to high activation of TNF signaling in VDZ non-remitters, anti-TNF treatment might represent a promising therapeutic strategy in VDZ refractory patients.
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Sex, Specimen part, Disease, Treatment, Subject
View SamplesOur aim was to identify genes that were differentially expressed in microglia stimulated with Lipopolysaccharide, Luteolin, or both.
Luteolin triggers global changes in the microglial transcriptome leading to a unique anti-inflammatory and neuroprotective phenotype.
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View SamplesPU.1 is a key transcription factor for macrophage differentiation. Novel PU.1 target genes were identified by mRNA profiling of PU.1-deficient progenitor cells (PUER) before and after PU.1 activation. We used two different types of Affymetrix DNA-microarrays (430 2.0 arrays and ST 1.0 exon arrays) to characterize the global PU.1-regulated transcriptional program underlying the early processes of macrophage differentiation.
Transcriptomic profiling identifies a PU.1 regulatory network in macrophages.
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View SamplesTo define the genes and pathways which are influenced by Foxp1 in the striatum at embryonic stage (E)18.5 we performed a microarray expression study comparing gene expression in striatal tissue from WT and Nestin-Cre (Foxp1-/-) animals.
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Specimen part
View SamplesThe pre-synaptic protein -synuclein is a key player in the pathogenesis of Parkinson's disease. Together with accumulation and missfolding of -synuclein protofibrils serve as seed structures for the aggregation of numerous proteins in the cytoplasm of neuronal cells, the so-called Lewy bodies. Furthermore, missense mutations in the SNCA gene and gene multiplications lead to autosomal dominant forms of familiar PD. However, so far the exact biological role of -synuclein in normal brain is elusive. To gain more insights into the biological function of this protein we monitored whole genome expression changes in dopaminergic neuroblastoma cells (SH-SY5Y) caused by a 90% reduction of -synuclein by RNA interference.
Microarray expression analysis of human dopaminergic neuroblastoma cells after RNA interference of SNCA--a key player in the pathogenesis of Parkinson's disease.
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View SamplesPigment Epithelium-Derived Factor (PEDF) has recently been identified as a factor that is significantly upregulated in late-stage osteoarthritic cartilage in which chondrocytes are confronted with terminal differentiation and cell death. Since PEDF is known to induce cell death of endothelial cells, it may also be responsible for terminal differentiation and cell death in cartilage.
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Specimen part, Disease
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