Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes - microarray study

ABSTRACT: Investigating the response of long non-coding RNA expression to LPS stimulation in human monocytes. This experiment is related to the RNA-seq study E-MTAB-2399.

ORGANISM(S): Homo sapiens

SUBMITTER: Nicholas Ilott

PROVIDER: E-MTAB-2408 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes

Project description:Investigating the response of long non-coding RNA expression to LPS stimulation in human monocytes. This experiment is related to the microarray study E-MTAB-2408.

2014-04-25 | E-MTAB-2399 | biostudies-arrayexpress

Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes.

Project description:Early reports indicate that long non-coding RNAs (lncRNAs) are novel regulators of biological responses. However, their role in the human innate immune response, which provides the initial defence against infection, is largely unexplored. To address this issue, here we characterize the long non-coding RNA transcriptome in primary human monocytes using RNA sequencing. We identify 76 enhancer RNAs (eRNAs), 40 canonical lncRNAs, 65 antisense lncRNAs and 35 regions of bidirectional transcription (RBT) that are differentially expressed in response to bacterial lipopolysaccharide (LPS). Crucially, we demonstrate that knockdown of nuclear-localized, NF-κB-regulated, eRNAs (IL1β-eRNA) and RBT (IL1β-RBT46) surrounding the IL1β locus, attenuates LPS-induced messenger RNA transcription and release of the proinflammatory mediators, IL1β and CXCL8. We predict that lncRNAs can be important regulators of the human innate immune response.

| S-EPMC4061460 | biostudies-literature

Long non-coding RNA landscape in human monocytes

Project description:We report the lncRNAs transcribed in the human primary monocyte cells. We performed deep RNA sequencing from four healthy individuals. In addition, the raw RNA-Seq data from 11 human monocyte samples were selected from public databases and generated a total ~1.7 billion reads. We identified ~ 8,000 lncRNAs from all the datasets of which more than 1,000 of them have not been previously reported in monocytes. We also validated a few of these novel lncRNAs in monocytes and other hematopoetic cell types. The other 11 datasets were taken from the following: ENCSR000CUC 6 samples E-MTAB-2399 4 samples GSM1526678 mRNA profiling of monocytes cells from 4 healthy individuals

2016-02-19 | E-GEOD-69753 | biostudies-arrayexpress

RNA-sequencing study of peripheral blood monocytes for chronic periodontitis

Project description:We confirmed immune response as the key mechanism and provided solid evidence for novel genes (e.g., FCAR and CUX1) and distinct biological processes (e.g., endocytosis, cytokine production and apoptosis) as potentially new important factors/mechanisms contributing to chronic periodontitis pathogenesis. We performed an RNA-sequencing (RNA-seq) study of peripheral blood monocytes (PBMs) in 5 non-smoking moderate to severe CP (case) subjects vs. 5 controls. We replicated the DEx transcripts/isoforms using an independent microarray dataset. We also pathway-based analysis on the identified/replicated DEx transcripts/isoforms using DAVID performed (Database for Annotation, Visualization and Integrated Discovery).

2016-07-16 | E-GEOD-61490 | biostudies-arrayexpress

Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes

Project description:Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes

| PRJEB5869 | ENA

Transcription profiling of monocytes from patients with autoimmune diabetes

Project description:Identifying a discriminating expression pattern of inflammatory genes in monocytes of patients with autoimmune diabetes

2008-08-01 | E-MEXP-1516 | biostudies-arrayexpress

Transcriptional profiling of monocytes of bipolar patients and controls

Project description:Bipolar disorder (BD) is a psychiatric disorder in which the core feature is pathological disturbance in mood ranging from extreme elation (mania) to severe depression. Study has shown an aberrant pro-inflammatory status of monocytes/macrophages in mood disorders. Therefore, this study aimed at studying the monocyte compartment in Bipolar Disorder, by transcription profiling of CD14+ monocytes in patients and controls.

2008-01-01 | E-MEXP-1275 | biostudies-arrayexpress

Transcription profiling of human osteoclastic differentiating from dendritic cells or monocytes

Project description:Comparison of osteoclastic differentiation pathway from DCs with the canonical differentiation pathway from monocytes by transcriptomic profiling

2009-09-01 | E-MEXP-2019 | biostudies-arrayexpress

The Paradigm of Macrophage Polarization is not Applicable per seto Human Circulating Monocytes

Project description:Macrophage activation is required for the control of innate and adaptive immune responses. The classification in M1 and M2 macrophages based on a combination of small numbers of membrane and soluble markers is operational in murine and human macrophages. If this classification may be extended to circulating monocytes is not elucidated. To answer such question, human monocytes were stimulated for 6 and 18 hours with IFN-gamma and IL-4, two canonical agonists of M1/M2 polarization in macrophages, and gene expression programs were investigated with whole genome microarrays. The temporal analysis of these programs showed marked differences to both IFN-gamma and IL-4. In 6-h stimulated monocytes, gene categories related to inflammatory and immune responses were enriched, and these monocytes exhibited a M1 and M2 polarization in response to IFN-gamma and IL-4, respectively, as found in macrophages. In 18-h stimulated monocytes, the categories related to innate immunity and metabolic pathways were enriched in response to IFN-gamma and IL-4, whereas PPAR signaling pathway was specifically enriched in response to IL-4. In addition, the M1 and M2 polarization induced by IFN-gamma and IL-4, respectively, was replaced by an original transcriptional program that did not depend on IFN-gamma and IL-4. This program appeared as networks around chemokines, NF-kappaB/MAP kinase pathways and MHC class II molecules. These results clearly demonstrated that monocyte activation consisted of an early polarized stage likely involved in effector responses and a delayed stage that may regulate host responses. The establishment of databases on human circulating monocytes using high throughput methods may be critical for pathophysiological and clinical non-invasive studies. Peripheral blood mononuclear cells (PBMCs) were isolated from leukopacks from normal blood donor buffy coats (Etablissement FranÃ§ais du Sang, Marseille, France) by Ficoll density gradient

2012-12-07 | E-GEOD-27658 | biostudies-arrayexpress

RNY (YRNA)-derived small RNAs regulate cell death and inflammation in monocytes/macrophages.

Project description:The recent discovery of new classes of small RNAs has opened unknown territories to explore new regulations of physiopathological events. We have recently demonstrated that RNY (or Y RNA)-derived small RNAs (referred to as s-RNYs) are an independent class of clinical biomarkers to detect coronary artery lesions and are associated with atherosclerosis burden. Here, we have studied the role of s-RNYs in human and mouse monocytes/macrophages and have shown that in lipid-laden monocytes/macrophages s-RNY expression is timely correlated to the activation of both NF-κB and caspase 3-dependent cell death pathways. Loss- or gain-of-function experiments demonstrated that s-RNYs activate caspase 3 and NF-κB signaling pathways ultimately promoting cell death and inflammatory responses. As, in atherosclerosis, Ro60-associated s-RNYs generated by apoptotic macrophages are released in the blood of patients, we have investigated the extracellular function of the s-RNY/Ro60 complex. Our data demonstrated that s-RNY/Ro60 complex induces caspase 3-dependent cell death and NF-κB-dependent inflammation, when added to the medium of cultured monocytes/macrophages. Finally, we have shown that s-RNY function is mediated by Toll-like receptor 7 (TLR7). Indeed using chloroquine, which disrupts signaling of endosome-localized TLRs 3, 7, 8 and 9 or the more specific TLR7/9 antagonist, the phosphorothioated oligonucleotide IRS954, we blocked the effect of either intracellular or extracellular s-RNYs. These results position s-RNYs as relevant novel functional molecules that impacts on macrophage physiopathology, indicating their potential role as mediators of inflammatory diseases, such as atherosclerosis.

| S-EPMC5386355 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data