Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CircRNA expression in idiopathic pulmonary fibrosis (IPF) and matched non-fibrotic plasma samples

ABSTRACT: We used circRNA microArray analysis from Arraystar to identify differential expression of circRNA in IPF patients compared to healthy controls.

ORGANISM(S): Homo sapiens

PROVIDER: GSE102660 | GEO | 2017/08/16

SECONDARY ACCESSION(S): PRJNA398329

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Human circRNA expression profiling in plasma sample of hepatocellular carcinoma

Project description:Arraystar Human circRNA Microarray is designed for the global profiling of human circRNAs. In this study, we applied a circRNA microarray to screen the potential biomarker for HCC. 20 samples extracted from plasma samples including HCC group before operation, and after operation, CH group and control group. Each group contained five samples.

2021-03-02 | E-MTAB-8799 | biostudies-arrayexpress

Idiopathic pulmonary fibrosis (IPF)

Project description:Idiopathic pulmonary fibrosis (IPF) is a disease related to AT2 cell. We used flow cytometry to analyze the epithelial component of donor and IPF lungs. From the live cells, we first excluded the CD31PosCD45Pos and then selected the EPCAMPos cells for further analysis using the human AT2 cell marker HTll-280 and the surface marker PD-L1. Our data indicate that, the bona fide differentiated AT2 cells (HTll-280High PD-L1Neg), were drastically reduced in the context of IPF. More interestingly, the number of HTll-280Low/Neg PD-L1High was drastically increased, suggesting that HTll-280Low PD-L1High epithelial cells could represent a pool of progenitors linked to the deficient AT2 lineage. The aim of this experiment is further characterization of AT2 and PDL1+ cells in donor and IPF.

2023-01-01 | GSE195770 | GEO

microRNA expression profiles in Idiopathic Pulmonary Fibrosis (IPF)

Project description:Idiopathic pulmonary fibrosis (IPF) is a lethal fibrotic lung disease characterized by enhanced fibroblast proliferation, collagen synthesis, extracellular matrix deposition. We obtained 28 IPF patient lung tissue samples from the Lung Tissue Research Consortium (LTRC). Here we determined the miRNA expression profiles in these IPF lung samples.

2019-04-02 | GSE129126 | GEO

Developmental programming in Idiopathic pulmonary fibrosis (IPF)

Project description:Global mRNA expression was compared between stable and progressive IPF using bronchoalveolar lavage derived mesenchymal stromal cells

2017-01-10 | GSE73854 | GEO

circRNA expression in HCC and matched non-tumor tissues

Project description:To determine the circRNA expression profile in HCC and matched non-tumor tissues, we used circRNA microArray analysis form Arraystar to examine the expression of circRNAs in HCC and matched non-tumor tissues.

2017-04-04 | GSE97332 | GEO

circRNA expression in CRC and matched non-tumor tissues

Project description:To determine the circRNA expression profile in CRC and matched non-tumor tissues, we used circRNA microArray analysis form Arraystar to examine the expression of circRNAs in CRC and matched non-tumor tissues.

2021-10-31 | GSE159669 | GEO

PLASMA biomarkers of Idiopathic Pulmonary Fibrosis

Project description:The aim of the current study is to find plasma-based biomarker candidates for Idiopathic Pulmonary Fibrosis (IPF). Incidence of IPF seems to be increasing in Europe and there is significant mortality associated with IPF. There are no sensistive biomarkers for IPF and diagnosis is entirely clinical and/or histopathological which is often delayed. Minimally invasive biomarkers of IPF would be expected to aid clinicians perfrom early diagnosis of IPF enabling better management of the disease.

2020-05-13 | PXD010965 | Pride

circRNA expression in infantile hemangioma (IH) and matched non-tumor tissues

Project description:To determine the circRNA expression profile in IH and matched non-tumor tissues, we uesed circRNA microArray analysis form Arraystar to examine the expression of circRNAs in IH and matched non-tumor tissues.

2019-05-09 | GSE98795 | GEO

Transcriptomic and epigenetic profiling of fibroblasts in Idiopathic Pulmonary Fibrosis (IPF)

Project description:ATAC-Seq was applied to identify differentially accessible regions within the genome between healthy and IPF fibroblasts.

2021-07-20 | GSE180242 | GEO

The profile of miRNAs in lung fibroblast-derived extracellular vesicles from idiopathic pulmonary fibrosis (IPF) patients or non-IPF individuals.

Project description:Accelerated senescence in lung epithelial cells is known to play a key role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). However, the exact mechanisms underlying the IPF-related epithelial cell phenotype have yet to be elucidated. Increasing evidence supports the concept that extracellular vesicles (EVs), including exosomes and microvesicles, mediate intercellular communication that contributes to diverse aspects of physiology and pathogenesis. Here, we demonstrate that lung fibroblasts (LFs) from IPF patients accelerate epithelial cell senescence via EV-mediated transfer of LF-derived pathogenic cargo to lung epithelial cells. Mechanistically, IPF LF-derived EVs increase mitochondrial reactive oxygen species (mtROS) and associated mitochondrial damage in lung epithelial cells, leading to mtROS-mediated activation of the DNA damage response and subsequent epithelial cell senescence. We show that IPF LF-derived EVs contain elevated levels of miR-23b-3p and miR-494-3p that are responsible for suppressing SIRT3, resulting in the EV-induced phenotypic changes of lung epithelial cells. Furthermore, we observe that miR-23b-3p and miR-494-3p expression increases in lung epithelial cells from IPF patients’ lungs. Finally, the levels of miR-23b-3p and 494-3p found in IPF LF-derived EVs correlate positively with IPF disease severity. These findings reveal that the accelerated epithelial cell mitochondrial damage and senescence observed during IPF pathogenesis are caused by a novel mechanism in which SIRT3 is suppressed by miR-containing EVs derived from IPF fibroblasts.

2020-08-04 | GSE124665 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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