Transcription profiling of human BE(2)-C neuronal responses to type I IFN stimulation
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: David Miller
PROVIDER: E-GEOD-16450 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series:; GSE16450: Human BE(2)-C neuronal responses to type I IFN stimulation; GSE16451: Human BE(2)-C neuronal responses to WEEV infection Experiment Overall Design: Refer to individual Series
2009-07-12 | E-GEOD-16452 | biostudies-arrayexpress
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Project description:To define probes which differentiate between the activity of type I or type II IFN, a human submandibular gland (HSG) cell line was cultured for 48 hours in the absence or presence of IFNa or IFNg. Gene expression was assayed at 4, 12, 24 or 48 hours and was compared to gene expression in untreated cells at each time point to define genes which are induced by type I or type II IFN. HSG cells were cultured for 2 days in the absence or presence of IFNa [1000U/ml] or IFNg [50ng/ml], and total RNA was isolated at 4, 12, 24, and 48 hours of culture. Details are in the Analytical Methods section of the manuscript: John C. Hall, Livia Casciola-Rosen, Alan E. Berger, Efstathia Kapsogeorgou, Chris Cheadle, Athanasios G. Tzioufas, Alan N. Baer, Antony Rosen,Precise probes of type II interferon activity define the origin of interferon signatures in target tissues in rheumatic diseases accepted for publication in PNAS (this GEO dataset will be released immediately upon electronic publication).
2012-10-08 | E-GEOD-41291 | biostudies-arrayexpress
Project description:Systemic lupus erythematosus (SLE) is characterized by increased vascular risk due to premature atherosclerosis independent of traditional risk factors. We previously proposed that interferon-? plays a crucial role in premature vascular damage in SLE. IFN-? alters the balance between endothelial cell apoptosis and vascular repair mediated by endothelial progenitor cells (EPCs) and myeloid circulating angiogenic cells (CACs). Here we demonstrate that IFN-? promotes an antiangiogenic signature in SLE and control EPCs/CACs, characterized by transcriptional repression of IL-1? and ?, IL-1 receptor 1 and vascular endothelial growth factor A (VEGF-A) and upregulation of IL-1 receptor antagonist (IL-1RN) and the decoy receptor IL1-R2. IL-1? promotes significant improvement in the functional capacity of lupus EPCs/CACs, therefore abrogating the deleterious effects of IFN-?. We used microarrays to analyze the effect of IFN? on peripheral blood EPCs/CACs and on bone marrow EPCs exposed to proangiogenic stimulation. Human healthy EPCs and CACs from PBMCs were isolated and cultured under proangiogenic stimulation; after IFNa incubation or not, RNA was extracted and processed for hybridization on Affymetrix microarrays.
2011-04-13 | E-GEOD-26949 | biostudies-arrayexpress
Project description:Systemic lupus erythematosus (SLE) is characterized by increased vascular risk due to premature atherosclerosis independent of traditional risk factors. We previously proposed that interferon-α plays a crucial role in premature vascular damage in SLE. IFN-α alters the balance between endothelial cell apoptosis and vascular repair mediated by endothelial progenitor cells (EPCs) and myeloid circulating angiogenic cells (CACs). Here we demonstrate that IFN-α promotes an antiangiogenic signature in SLE and control EPCs/CACs, characterized by transcriptional repression of IL-1α and β, IL-1 receptor 1 and vascular endothelial growth factor A (VEGF-A) and upregulation of IL-1 receptor antagonist (IL-1RN) and the decoy receptor IL1-R2. IL-1β promotes significant improvement in the functional capacity of lupus EPCs/CACs, therefore abrogating the deleterious effects of IFN-α. We used microarrays to analyze the effect of IFNα on peripheral blood EPCs/CACs and on bone marrow EPCs exposed to proangiogenic stimulation. Human healthy EPCs from bone marrow were isolated and cultured under proangiogenic stimulation; after IFNa incubation or not, RNA was extracted and processed for hybridization on Affymetrix microarrays.
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Project description:We report the IFN-induced dynamics in murine splenic B cells. Male C57BL/6 mice were injected subcutaneously with 10,000U IFNa and spleens were removed at 90min. B cells were negatively isolated using magnetic beads and profiled for the chromatin configuration by ATAC-seq. Profilings of chromatin configuration by ATAC-seq (0 and 90min, biological duplicate for each).
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Project description:Analysis of transcription response of undifferentiated human BE(2)-C neuronal cells to stimulation with novel indole-2-carboxamide antivirals 205432 or 206381. Independent sets of BE(2)-C cells were treated with 25 uM of either 205432 or 206381, or DMSO as control. Total RNA was harvested at 24 h after stimulation and analyzed with Affymetrix U133 Plus 2.0 chips.
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Project description:Systemic lupus erythematosus (SLE) is characterized by increased vascular risk due to premature atherosclerosis independent of traditional risk factors. We previously proposed that interferon-α plays a crucial role in premature vascular damage in SLE. IFN-α alters the balance between endothelial cell apoptosis and vascular repair mediated by endothelial progenitor cells (EPCs) and myeloid circulating angiogenic cells (CACs). Here we demonstrate that IFN-α promotes an antiangiogenic signature in SLE and control EPCs/CACs, characterized by transcriptional repression of IL-1α and β, IL-1 receptor 1 and vascular endothelial growth factor A (VEGF-A) and upregulation of IL-1 receptor antagonist (IL-1RN) and the decoy receptor IL1-R2. IL-1β promotes significant improvement in the functional capacity of lupus EPCs/CACs, therefore abrogating the deleterious effects of IFN-α. We used microarrays to analyze the effect of IFNα on peripheral blood EPCs/CACs and on bone marrow EPCs exposed to proangiogenic stimulation. Human lupus EPCs and CACs from PBMCs were isolated and cultured under proangiogenic stimulation; after IFNa incubation or not, RNA was extracted and processed for hybridization on Affymetrix microarrays.
2011-04-13 | E-GEOD-26950 | biostudies-arrayexpress
Project description:Interferon tau (IFNT), a Type I IFN similar to alpha IFNs (IFNA), is the pregnancy recognition signal, produced by the ruminant conceptus. To elucidate specific effects of bovine IFNT and of other conceptus-derived factors, endometrial gene expression changes during early pregnancy were compared to gene expression changes after intrauterine application of human IFNA2. In study one, endometrial tissue samples were obtained on days (D) 12, 15, and 18 post-mating from nonpregnant or pregnant heifers. In study two, heifers were treated from D14 to D16 of the estrous cycle with an intrauterine device releasing IFNA2 or placebo lipid extrudates or PBS only as controls. Endometrial biopsies were collected after flushing the uterus. All samples from both experiments were analyzed with an Affymetrix Bovine Genome Array. Study one revealed differential gene expression between pregnant and nonpregnant endometria on D15 and D18. In study two, IFNA2 treatment resulted in differential gene expression in the bovine endometrium. Comparison of the datasets from both studies identified genes that were differentially expressed in response to IFNA2 but not in response to pregnancy on D15 or D18. Vice versa, genes were found as differentially expressed during pregnancy but not after IFNA2 treatment. In study three, spatiotemporal alterations in expression of selected genes were determined in uteri from nonpregnant and early pregnant heifers using in situ hybridization. The findings of this study suggest differential effects of bovine IFNT compared to human IFNA2 and that some pregnancy-specific changes in the endometrium are elicited by conceptus-derived factors other than IFNT. Study I: Early pregnancy; day 12 of pregnancy (n=5 heifers), day 15 of pregnancy (n=3), day 18 of pregnancy (n=4), day 12 cyclic controls (n=5), day 15 cyclic controls (n=3), day 18 cyclic controls (n=4). Study II: Treatment with human interferon alpha (IFNA); IFNA treatment group (IFNA, n=3 heifers), placebo group (PLAC, n=3 heifers), control group (CONT, n=3 heifers).
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