TNF-M-NM-1 treated HUVECs: microRNA negative control VS. miR-181b
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Mark Feinberg
PROVIDER: E-GEOD-35030 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Transcriptional profiling of TNF-α treated HUVECs comparing cells transfected microRNA negative control with cells transfected with miR-181b.
2012-05-16 | GSE35030 | GEO
Project description:Endothelial cells are critical for angiogenesis, and microRNAs plays important roles in this process. We investigated the regulatory role of microRNAs in endothelial cells of hepatocellular carcinoma (HCC) by examining the microRNA expression profile of human umbilical vein endothelial cells (HUVECs) in the absence or presence of human HCC cells, and identified miR-146a as the most highly up-regulated microRNA. Furthermore, we revealed that miR-146a promoted the expression of platelet-derived growth factor receptor (PDGFRA) in HUVECs, and this process was mediated by BRCA1. Overexpression of PDGFRA in the ECs of HCC tissues was associated with microvascular invasion, and predicted a poorer prognosis. These results suggest that MiR-146a plays a key role in regulating the angiogenic activity of ECs in HCC through miR-146a-BRCA1-PDGFRA pathway. MiR-146a may emerge as a potential anti-angiogenic target on ECs for HCC therapy. We have employed whole genome OneArray to examine the genome expression changes of HUVECs overexpressing miR-146a.
2013-04-13 | E-GEOD-46022 | biostudies-arrayexpress
Project description:mRNA expression after Ezh2 knock down was analyzed to identify genes regulated by Ezh2. Human umbilical vein endothelial cells (HUVEC) were transfected with 25 nmol/L of control small interfering RNA (siRNA) (Silencer Select Negative Control Ambion, Austin, TX) or siRNA directed against Ezh2 (s4918; Ambion) using Oligofectamine (Invitrogen). Total RNA was harvested 72 hours after transfection.
2012-10-16 | E-GEOD-41610 | biostudies-arrayexpress
Project description:TNF-α treated HUVECs: microRNA negative control VS. miR-181b
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Project description:Bone marrow-derived mast cells were derived from three different female C57Bl/6 mice of similar age. Cells were transduced with pAPM lentiviruses either overexpressing microRNA-221 or a non functional microRNA-221 mutant, termed miR-221m, where four point-mutations were introduced in the seed sequence of miR-221. The samples overexpressing miR-221m were used as references for the corresponding miR-221 overexpressing BMMCs from the same mouse (mouse matched reference). The experiment was performed in order to gain more insights about the molecular mechanisms underlying miR-221 effects in mast cells. Two-condition experiment, BMMC overexpressing miR-221 vs BMMC overexpressing miR-221m. Biological replicates: 3 replicates overexpressing miR-221, 3 control replicates overexpressing miR-221m.
2011-11-23 | E-GEOD-24462 | biostudies-arrayexpress
Project description:The Epstein Barr virus (EBV) encoded latent membrane protein-1 (LMP1) is a functional homologue of the tumor necrosis factor receptor family and contributes substantially to the oncogenic potential of EBV through activation of Nuclear Factor-kappaB (NF-kappaB). MicroRNAs (miRNAs) are a class of small RNA molecules that are involved in the regulation of cellular processes such as growth, development, and apoptosis, and have recently been linked to cancer phenotypes. Through miRNA microarray analysis, we demonstrate that LMP1 dysregulates the expression of several cellular miRNAs, including the most highly regulated of these, miR-146a. Quantitative RT-PCR analysis confirmed induced expression of miR-146a by LMP1. Analysis of miR-146a expression in EBV latency type III and type I cell lines revealed substantial expression of miR-146a in type III (which express LMP1) but not in type I cell lines. Reporter studies demonstrated that LMP1 induces miR-146a predominantly through two NF-kappaB binding sites in the miR-146a promoter and identified a role for an OCT-1 site in conferring basal and induced expression. Array analysis of cellular mRNAs expressed in Akata cells transduced with an miR-146a expressing retrovirus identified genes that are directly or indirectly regulated by miR-146a, including a group of interferon responsive genes that are inhibited by miR-146a. Since miR-146a is known to be induced by agents that activate the interferon response pathway (including LMP1), these results suggest that miR-146a functions in a negative feedback loop to modulate the intensity and/or duration of the interferon response. Keywords: Analysis of gene expression changes altered by the microRNA, miR-146a EBV positive Burkitt's lymphoma cell line, Akata, was infected with the control retrovirus, pEhyg, or the miR-146a expressing retrovirus, pEhyg-miR-146a. Two infections were carried out for control retrovirus and two infections were carried out with the pEhyg-miR-146a retrovirus. Total RNA was prepared from each of the 4 infections. Control and miR-146a infection set 1 was subjected to dual color array analysis on chip 1. Control and miR-146a infection set 2 was subjected to dual color array analysis on second array of chip 1. Dye swaps of each of these were carried out on two arrays from a second chip (chip 2).
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Project description:To investigate machanism of miR-210-3p regulating angiogenic ability of human umbilical vein endothelial cells (HUVECs) in hypoxic conditions, we transfected miR-210-3p mimic to overexpress miR-210-3p in human umbilical vein endothelial cells. We than performed RNA sequencing of miR-210-3p mimic-transfected and control HUVECs under hypoxic conditions to evaluate the transcriptional changes in the miR-210-3p-overexpressing HUVECs.
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Project description:Hepatic encephalopathy (HE) is a frequent complication of liver cirrhosis and is seen as the clinical manifestation of a low grade cerebral edema associated with oxidative-nitrosative stress, however, comprehensive data on HE-associated molecular derangements in human brain are lacking. In the present study we used a whole human genome micro-array approach for gene expression profiling in post mortem brain samples from cirrhotic patients with or without HE and non-cirrhotic controls. Altered expression levels were found for a total of 1012 genes in liver cirrhotic patients without and with HE and HE-characteristic gene expression changes were identified. Genes with altered expression pattern in HE were related oxidative stress, microglia activation, inflammatory signalling pathways, cellular proliferation and apoptosis. Despite an up-regulation of genes associated with microglia activation, pro-inflammatory cytokine mRNA profiles remained unchanged in the brain of patients with liver cirrhosis and HE as compared to controls. Interestingly, many genes counteracting pro-inflammatory signalling and inflammatory cytokine expression were up-regulated in the cerebral cortex of patients with liver cirrhosis and HE. It is concluded that pathogenetic mechanisms of HE deduced from cell culture and animal experiments, such as oxidative stress, altered Zn2+-homeostasis and microglia activation also apply to human brain from cirrhotic patients with HE. The study also revealed a not yet recognized increased expression of genes antagonizing pro-inflammatory signalling and inflammatory cytokine expression. The dataset comprises 19 samples divided into three sample groups each representing a certain liver disease condition of humans.
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Project description:Plasmacytoid dendritic cells (PDC) play an important role in innate and adaptive immunity and were shown to be identical to previously described natural IFN-M-NM-1-producing cells (NIP). Here, we describe two functionally distinct PDC subpopulations that are characterized by the differential expression of stem cell antigen-1 (Sca-1; Ly-6A/E). Sca-1- PDC are mainly found in the bone marrow, appear first during development, show a higher proliferative activity and represent the more precursor phenotype. Sca-1+ PDC are mostly located in secondary lymphoid organs and show higher expression of MHC class II molecules. Sca-1- PDC give rise to a Sca-1+ subset upon activation or in response to tissue-specific factors. Interestingly, in contrast to Sca-1- PDC, Sca-1+ PDC are defective in type I IFN production upon endosomal TLR9 stimulation, whereas lysosomal signaling via TLR9 is functional in both subsets. Gene expression analysis revealed that osteopontin (Opn) is strongly upregulated in Sca-1- PDC. This data provides evidence for the molecular basis of the observed functional heterogeneity, as the intracellular isoform of Opn couples TLR9 signaling to IFN-M-NM-1 expression. Taken together, our results indicate that Sca-1- PDC are an early developmental stage of PDC with distinct innate functions representing the true murine NIP. The dataset comprises eight samples divided into two sample groups consisting of Sca-1(-) and Sca-1(+) PDCs collected from in vitro culture of differentiated bone marrow precursor cells using mFlt3-L
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Project description:We used whole genome transcriptome as gene discovery to further understand the differential behaviour of the first (embryonic) and second waves of thymic settling progenitors in the murine embryo. Mouse embryos at days 13 and 18 of gestation were isolated and the thymic lobes were dissected. Single cell suspension was prepared and treated with biotinilated antibodies to CD3, CD4, CD8, TER119, Gr1, CD25, CD19, NK1.1 and CD11c. Cell suspensions were then incubated with streptavidin Miltenyi Macs beads. Lineage negative thymocytes were recovered in Macs columns. Cell suspensions were then incubated with antibodies against CD135, CD117, CD44, CD24 and Streptavidin bound to PECy7. Lin-, CD117+, CD44+, CD24low, CD135+ cells were then isolated by cell sorting. 3 biological replicates of each sample were isolated with 104-3x104 cells
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