Twenty-one genes (27 probe sets) were up-regulated in CAF, as compared with NF. Known functions of these genes relate to paracrine or intracellular signaling, transcriptional regulation, extracellular matrix and cell adhesion/migration. Ten genes (14 probe sets) were down-regulated in CAF, including the pluripotency transcription factor KLF4. Quantitative RTPCR analysis of 10 genes validated the array results. Immunohistochemical staining for three gene products confirmed stromal expression in terms of location and relative quantity. Surprisingly, the variability of gene expression was slightly higher in NF than in CAF, suggesting inter-individual heterogeneity of normal stroma.
Heterogeneity of gene expression in stromal fibroblasts of human breast carcinomas and normal breast.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Chronic exposure to cigarette smoke condensate in vitro induces epithelial to mesenchymal transition-like changes in human bronchial epithelial cells, BEAS-2B.
Treatment
View SamplesBEAS-2B cells have been treated with low doses (20g/ml) of CSC for 4 months. As negative control BEAS-2B cells were treated with DMSO (the CSC solvent). Non-treated cells were cultivated in parallel.
Chronic exposure to cigarette smoke condensate in vitro induces epithelial to mesenchymal transition-like changes in human bronchial epithelial cells, BEAS-2B.
Treatment
View SamplesThe study seeks to identify the epigenetic changes caused by exposure of to cigarette smoke condensate. To this goal human bronchial epithelial cells, BEAS-2B, were treated with 5-aza-2deoxycitidine and trychostatin A (5AzaC/TSA) subsequent to a chronic exposure (1 month) to cigarette smoke condensate (CSC). As negative control served BEAS-2B cells that were untreated or treated with CSC/DMSO for one month without the subsequent application of 5Aza/TSA.
Chronic exposure to cigarette smoke condensate in vitro induces epithelial to mesenchymal transition-like changes in human bronchial epithelial cells, BEAS-2B.
Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Malignant catarrhal fever of cattle is associated with low abundance of IL-2 transcript and a predominantly latent profile of ovine herpesvirus 2 gene expression.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Induction of the nuclear receptor PPAR-γ by the cytokine GM-CSF is critical for the differentiation of fetal monocytes into alveolar macrophages.
No sample metadata fields
View SamplesWe hypothesized that the relative abundances of host cell transcripts in lymph nodes of animals with malignant catarrhal fever (MCF), compared to healthy controls, may be used to identify pathways that may help to explain the pathogenesis of MCF. Therefore, an abundance of host cell gene expression patterns in lymph nodes of animals with MCF and healthy controls were analyzed by microarray. Indeed, a vast number of genes related to inflammatory processes, lymphocyte activation, cell proliferation and apoptosis were detected at different abundances. However, the IL-2 transcript was eminent among the transcripts, which were, compared to healthy controls, less abundant in animals with MCF. Compared to healthy cattle, bovines with MCF appear to mimic an IL-2 knockout phenotype that has been described in mice. This supports the hypothesis that immunopathogenic events are linked to the pathogenesis of MCF. IL-2-deficiency may play an important role in the process.
Malignant catarrhal fever of cattle is associated with low abundance of IL-2 transcript and a predominantly latent profile of ovine herpesvirus 2 gene expression.
No sample metadata fields
View SamplesTissue-resident macrophages comprise heterogeneous populations with unique functions and distinct gene expression signatures. While it has been established that they mostly originate from embryonic progenitors, the signals inducing a characteristic tissue-specific differentiation program remain unknown. Here we identify PPAR as the crucial transcription factor determining perinatal alveolar macrophage (AM) development and identity. Development of the fetal monocyte derived AM precursor was largely abrogated in CD11c-Cre/Ppargfl/fl mice. To reveal the underlying changes in gene expression, we performed microarray analysis of sorted WT and KO AM and pre-AM from 3 different timepoints.
Induction of the nuclear receptor PPAR-γ by the cytokine GM-CSF is critical for the differentiation of fetal monocytes into alveolar macrophages.
No sample metadata fields
View SamplesTissue-resident macrophages comprise heterogeneous populations with unique functions and distinct gene expression signatures. While it has been established that they mostly originate from embryonic progenitors, the signals inducing a characteristic tissue-specific differentiation program remain unknown. Here we identify PPAR as the crucial transcription factor determining perinatal alveolar macrophage (AM) development and identity. Development of the fetal monocyte derived AM precursor was largely abrogated in CD11c-Cre/Ppargfl/fl mice. To reveal the underlying changes in gene expression, we performed microarray analysis of sorted WT and KO AM and pre-AM from 3 different timepoints.
Induction of the nuclear receptor PPAR-γ by the cytokine GM-CSF is critical for the differentiation of fetal monocytes into alveolar macrophages.
No sample metadata fields
View SamplesChronic infection with the bacterial pathogen Helicobacter pylori is a risk factor for the development of gastric cancer, yet remains asymptomatic in a majority of individuals. We report here that the C57Bl6 mouse model of experimental infection with the closely related H. felis recapitulates this wide range in host susceptibility. A majority of infected mice develop premalignant lesions such as gastric atrophy, compensatory epithelial hyperplasia and intestinal metaplasia, whereas a minority is completely protected from preneoplasia. Protection is associated with the failure to mount an IFN-gamma response to the infection and an associated high Helicobacter burden. We demonstrate that IFN-gamma is essential for clearance of Helicobacter, but also mediates the formation of preneoplastic lesions. We further provide evidence that IFN-gamma triggers a specific transcriptional program in murine gastric epithelial cells in vitro and in vivo, and induces their preferential transformation to the hyperplastic phenotype. In summary, our data suggest a dual role for IFN-gamma in Helicobacter pathogenesis that could provide an explanation for the differential susceptibility to H. pylori-induced gastric pathology in the human population.
The CD4+ T cell-mediated IFN-gamma response to Helicobacter infection is essential for clearance and determines gastric cancer risk.
Treatment
View Samples