Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

IL-1B mediated adaptive reprogramming of endogenous human cardiac fibroblast to cells with immune features during fibrotic remodelling

ABSTRACT: IL-1B mediated adaptive reprogramming of endogenous human cardiac fibroblast to cells with immune features during fibrotic remodelling

PROVIDER: PRJNA803885 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18110671_1.fastq.gz	Fastqsanger.gz
	SRR18110671_2.fastq.gz	Fastqsanger.gz
	SRR18110672_1.fastq.gz	Fastqsanger.gz
	SRR18110672_2.fastq.gz	Fastqsanger.gz
	SRR18110673_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 19

Similar Datasets

IL-1B mediated adaptive reprogramming of endogenous human cardiac fibroblast to cells with immune features during fibrotic remodelling

Project description:We profile the transcriptome of a unique sub-population of primary human ventricular cardiac fibroblast (hVCFs) cells expressing dual mesenchymal and lymphoidal features in response to cytokines specifically, IL-1B using next-generation sequencing (NGS). The goals of the project are to 1) compare and contrast novel CD4+ cells with CD4- human cardiac fibroblast cells; 2) identify and classify the novel subpopulation of cells from the heart based on the expression of lineage specific markers, and markers associated with plasticity, morphogenesis, homeostasis, metabolism and signaling pathways. hVCFs were sorted based on the expression of CD4 markers classified as CD4+ and CD4- cell population. After initial samples QC analysis, RNA libraries were prepared with polyA selection and sequenced on Illumina in 2x150bp paired end configuration. About 35M paired reads per samples for 10 samples or 58M paired reads per samples for 6 samples were obtained for 3 biological replicates. This study provides genetic signatures of newly identified sub-population of human cardiac fibroblasts and response to pro-inflammatory cytokines critical to cardiac remodeling and heart failure.

2023-09-28 | GSE196195 | GEO

Antigen-independent stimulation of effector CD4+ T cells protects from fibrotic remodelling in myocarditis

Project description:Antigen-independent stimulation of effector CD4+ T cells protects from fibrotic remodelling in myocarditis

| PRJEB28775 | ENA

IL-1β-mediated adaptive reprogramming of endogenous human cardiac fibroblasts to cells with immune features during fibrotic remodeling.

Project description:The source and roles of fibroblasts and T-cells during maladaptive remodeling and myocardial fibrosis in the setting of pulmonary arterial hypertension (PAH) have been long debated. We demonstrate, using single-cell mass cytometry, a subpopulation of endogenous human cardiac fibroblasts expressing increased levels of CD4, a helper T-cell marker, in addition to myofibroblast markers distributed in human fibrotic RV tissue, interstitial and perivascular lesions in SUGEN/Hypoxia (SuHx) rats, and fibroblasts labeled with pdgfrα CreERt2/+ in R26R-tdTomato mice. Recombinant IL-1β increases IL-1R, CCR2 receptor expression, modifies the secretome, and differentiates cardiac fibroblasts to form CD68-positive cell clusters. IL-1β also activates stemness markers, such as NANOG and SOX2, and genes involved in dedifferentiation, lymphoid cell function and metabolic reprogramming. IL-1β induction of lineage traced primary mouse cardiac fibroblasts causes these cells to lose their fibroblast identity and acquire an immune phenotype. Our results identify IL-1β induced immune-competency in human cardiac fibroblasts and suggest that fibroblast secretome modulation may constitute a therapeutic approach to PAH and other diseases typified by inflammation and fibrotic remodeling.

| S-EPMC10673909 | biostudies-literature

EZH2-dependent transcriptional complex promotes aberrant epithelial remodelling after injury

Project description:Unveiling the molecular mechanisms of tissue remodelling following injury is imperative to elucidate its regenerative capacity and aberrant repair in disease. Using different omics approaches, we identified enhancer of zester homolog 2 (EZH2) as a key regulator that initiates a fibrotic cascade in injured lung epithelium. Epithelial-injury-driven enrichment of nuclear transforming growth factor-b-activated kinase 1 (TAK1) mediates EZH2 phosphorylation to facilitate the release of EZH2 from polycomb repressive complex 2 (PRC2). This process leads to the establishment of a fibrotic transcriptional complex of EZH2, RNA-polymerase II (POL2) and nuclear actin, which orchestrates aberrant epithelial lung repair programs. The liberation of EZH2 from PRC2 is accompanied by an EZH2-EZH1 switch to preserve silencing at non-target genes. Loss of epithelial TAK1, EZH2 or blocking nuclear actin influx attenuates the fibrotic cascade and restores respiratory homeostasis. Accordingly, EZH2 inhibition significantly improves outcomes in a pulmonary fibrosis mouse model. Our results reveal an important non-canonical function of EZH2, paving the way for new therapeutic interventions in fibrotic lung diseases.

2021-04-27 | MSV000087321 | MassIVE

Single-cell RNA-seq reveals fibroblast heterogeneity and increased mesenchymalfibroblastsin human skin fibrotic diseases

Project description:Skin fibrotic disease representsa major global healthcare burden, characterized by fibroblast hyperproliferation and excessive accumulation of extracellular matrix.Fibroblasts are found to be heterogeneous in multiple fibrotic diseases,but the fibroblast heterogeneity of skin fibrotic diseases remains unknown.In this study, we performed single-cell RNA-seq in keloid, a paradigm of skin fibrotic diseases, andnormal scardermis tissues.Our results indicate that keloid and normal scar fibroblasts could be divided into 4 subpopulations: secretory-papillary, secretory-reticular, mesenchymal and pro-inflammatory.The percentage of mesenchymal fibroblast subpopulationincreased significantly in keloid compared to normal scar. Interestingly, we also found increasing mesenchymal fibroblast subpopulation in scleroderma, another skin fibrotic disease.Function studies showed that the mesenchymal fibroblasts promoted collagen synthesis of the other fibroblasts in keloid partiallythrough secreting POSTN. These findings will help us understandskin fibroticpathogenesis in depth,and provided potential target cells for fibrotic diseases therapies.

2021-05-23 | GSE163973 | GEO

Tenacibaculum sp. 1B UA strain:1B UA

Project description:Tenacibaculum sp. 1B UA strain:1B UA Genome sequencing and assembly

| PRJNA810982 | ENA

Fibrotic Remodelling of Epicardial Adipose Tissue in Patients with Atrial Fibrillation: Comparative Analyses of Histological Findings and Computed Tomographic Imaging

Project description:Aims: We tested the hypothesis that central-marginal dispersion in adipocyte diameter in epicardial adipose tissue (EAT) would represent fibrotic remodelling of EAT, a crucial state to promote atrial myocardial fibrosis to form a substrate of atrial fibrillation (AF). We also investigated whether the central-marginal EAT density ratio by the analyses of computed tomographic (CT) imaging could predict the central-marginal adipocyte diameter ratio in EAT. Methods and results: Left atrial appendage samples were obtained from 76 consecutive AF patients during cardiovascular surgery. EAT at central area (Central EAT) and that adjacent to atrial myocardium (Marginal EAT) were evaluated. Compared to the Central EAT, the dimeter of adipocytes was smaller, fibrotic remodeling of EAT (EAT fibrosis) was more severe, and the infiltration of CD3-, CD68-, or α-SMA-positive cells were more abundant in the Marginal EAT. EAT fibrosis positively correlated with adipocyte diameter in the Central EAT, while it negatively correlated with that in the Marginal EAT, resulting in the tightly positive correlation between EAT fibrosis and the ratio of central to marginal adipocyte diameter (C/M diameter ratio) (r=0.73, p<0.01). The C/M diameter ratio was greater in patients with persistent AF (PeAF) than in those with paroxysmal AF (PAF) (p<0.01). The CT density in Central EAT and Marginal EAT was measured and their ratio (C/M density ratio) was calculated. The C/M density ratio correlated tightly with the C/M diameter ratio (r=0.69, p<0.01). Conclusion: Our results suggest that C/M adipocyte diameter ratio was associated with fibrotic remodeling of EAT and progression of AF. Our results also suggest that C/M adipocyte diameter ratio could be accurately predicted by the analyses of CT findings noninvasively.

2021-08-25 | GSE154436 | GEO

Raoultella ornithinolytica strain:B1645-1B | isolate:B1645-1B

Project description:Raoultella ornithinolytica strain:B1645-1B | isolate:B1645-1B Genome sequencing

| PRJNA1000043 | ENA

Transcription profiling of human primary hematopoietic CD34+ cells to investigate Growth Factor Independence-1B (Gfi-1B) functions

Project description:Growth Factor Independence-1B (Gfi-1B) is a transcriptional repressor essential for erythropoiesis and megakaryopoiesis. Targeted gene disruption of Gfi-1B in mice leads to embryonic lethality due to failure to produce definitive erythrocytes, hindering the study of Gfi-1B function in adult hematopoiesis. We here show that, in humans, Gfi-1B controls the development of erythrocytes and megakaryocytes by regulating the proliferation and differentiation of bipotent erythro-megakaryocytic progenitors (MEP). We further identify in this cell population the type III transforming growth factor-? receptor gene, TGFBR3, as a direct target of Gfi-1B. Knock down of Gfi-1B results in altered TGF? signaling as shown by the increase in Smad2 phosphorylation and its inability to associate to the Transcription Intermediary Factor 1? (TIF1?). Because Smad2/TIF1? complex is known to specifically regulate erythroid differentiation, we propose that, by repressing the transforming growth factor-? receptor III (T?R?II) expression, Gfi-1B favors the Smad2/TIF1? interaction downstream of TGF? signaling, allowing immature progenitors to differentiate toward the erythroid lineage.

2010-04-19 | E-MEXP-2560 | biostudies-arrayexpress

Functional Pdgfra fibroblast heterogeneity in normal and fibrotic mouse lung

Project description:Using, scRNA Seq transcriptomic analysis, we report that Pdgra+ fibroblasts in mouse lung have significant heterogenity in normal and fibrotic lung, and key pathways involved in lipogenic and fibrogenic pathways govern the transition of normal lipofibroblasts from a normal to a myofibroblast phenotype following lung injury

2023-10-19 | GSE183423 | GEO

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