Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis of lung fibroblasts from 5 control and 5 IPF patients with/out TGF-b1 stimulation

ABSTRACT: Isolated primary human fibroblasts from 5 control and 5 IPF patients were treated with/out 3ng/ml TGF-b1 for 24 hours before cells were lysed for RNA extraction.

ORGANISM(S): Homo sapiens

PROVIDER: GSE129164 | GEO | 2019/04/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome analysis of lung fibroblasts from 5 control and 5 IPF patients with/out TGF-b1 stimulation

Project description:Transcriptome analysis of lung fibroblasts from 5 control and 5 IPF patients with/out TGF-b1 stimulation

| PRJNA530261 | ENA

Therapeutic activity of GARP:TGF-b1 blockade in murine primary myelofibrosis

Project description:Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by clonal expansion of myeloid cells, notably megakaryocytes (MKs), and aberrant cytokine production leading to bone marrow (BM) fibrosis and insufficiency. Current treatment options are limited. TGF-b1, a profibrotic and immunosuppressive cytokine, is involved in PMF pathogenesis. While all cell types secrete inactive, latent TGF-b1, only a few activate the cytokine via cell type-specific mechanisms. The cellular source of the active TGF-b1 implicated in PMF is not known. Transmembrane protein GARP binds and activates latent TGF-b1 on the surface of regulatory T lymphocytes (Tregs) and MKs or platelets. Here, we found increased expression of GARP in BM and spleen of mice undergoing PMF and tested the therapeutic potential of a monoclonal antibody that blocks TGF-b1 activation by GARP-expressing cells. GARP:TGF-b1 blockade reduced not only fibrosis, but also clonal expansion of transformed cells. Using mice carrying a genetic deletion of Garp in either Tregs or MKs, we found that the therapeutic effects of GARP:TGF-b1 blockade in PMF imply targeting GARP on Tregs. These therapeutic effects, accompanied by increased IFN-g signals in the spleen, were lost upon CD8 T cell depletion. Our results suggest that selective blockade of TGF-b1 activation by GARP-expressing Tregs increase a CD8 T cell-mediated immune reaction that limits transformed cell expansion, providing a novel approach that could be tested to treat patients with myeloproliferative neoplasms.

2022-10-27 | GSE216221 | GEO

Secretomics of TGF-B1-stimulated IMR-90 cells with and without sanglifehrin A

Project description:Proteins secreted from TGF-B1-stimulated IMR-90 cells with and without sanglifehrin A were profiled.

2024-10-17 | PXD029541 | Pride

Transcription profiling of mouse mammary epithelial cells NMuMG treatd with TGF-b1 - time series experiment

Project description:Response of mouse mammary epithelial cells NMuMG to TGF-b1 - time course experiment. Identification of novel gene targets involved in TGF-b1-driven regulation of epithelial-mesenchymal transition (EMT).

2004-10-01 | E-MEXP-139 | biostudies-arrayexpress

Cardiac-derived TGF-b1 confers resistance to diet-induced obesity through regulation of adipocyte size and function.

Project description:Regulation of organismal homeostasis in response to nutrient availability is a vital physiological process that involves inter-organ communication. Understanding the mechanisms controlling systemic cross talk for maintenance of metabolic health is critical to counteract diet-induced obesity. Here, we show that cardiac-derived transforming growth factor beta 1 (TGF-b1) protects against weight gain and glucose intolerance in mice subjected to high-fat diet. Secretion of TGF-b1 by cardiomyocytes correlates with bioavailability of this factor in circulation. TGF-b1 prevents adipose tissue inflammation independent of body weight and glucose metabolism phenotypes, suggesting protection from adipocyte dysfunction-driven immune cell recruitment. TGF-b1 alters gene expression programs in white adipocytes, favoring their thermogenic fate and consequently increasing their mitochondrial oxygen consumption rates. Ultimately, subcutaneous and visceral white adipose tissue from heart-specific TGF-b1 transgenic mice fail to undergo cellular hypertrophy, leading to reduced overall adiposity during high-fat feeding. Thus, TGF-b1 is a critical mediator of heart-fat communication for regulation of systemic metabolism.

2021-11-03 | GSE179102 | GEO

Gene expression profile of human peritoneal mesothelial cells (HPMC) treated with TGF-b1

Project description:Long-term peritoneal dialysis is associated with progressive fibrosis of the peritoneum. Epithelial-mesenchymal transition (EMT) of mesothelial cells is an important mechanism involved in peritoneal fibrosis, and TGF-b1 is considered central in this process. We conducted network-based integrated analysis of transcriptomic data to systemically characterize the molecular signature of TGF-b1-stimulated human peritoneal mesothelial cells (HPMCs).

2018-10-18 | GSE121372 | GEO

Comparison of the LIGHT and TGF-B1 induced transcriptomes in esophageal FBL

Project description:To understand the transcriptional responses induced by LIGHT in esophageal fibroblasts and compare them to the pro-fibrotic TGF-B1

2020-08-03 | GSE143482 | GEO

IL-2 and TGF-b1 promote regulatory activity in NK cells following Hematopoietic Stem Cell Transplantation

Project description:Natural Killer(NK) cell activity is influenced by cytokines and microenvironment factors, resulting in remarkably diverse functions ranging from contributing to inflammatory responses to instead inhibiting T cell and B cell activity, thereby serving as rheostats of adaptive immunity. Using scRNAseq, we identified a TGFb1highCD56brightNK cell population associated with protection from acute Graft-versus-Host Disease. We further define a role for the combination of IL-2 and TGF-b in promoting NK cells to acquire a regulatory phenotype. ‘Induced’ regulatory NK cells produce high amounts of TGF-b1, inhibited T cells, could promote naïve T cells differentiation into regulatory T cells, and exhibited a unique transcriptional program that includes expression of IKZF2(HELIOS) and ZNF683(HOBIT). This phenotype was not stable, and induced regulatory NK cells lost the ability to secrete TGF-b1 upon exposure to different cytokines. These findings define protective CD56brightNK cells in Hematopoietic Stem Cell Transplant, and support IL-2 and TGF-b1 promote regulatory NK cells.

2024-11-12 | GSE255298 | GEO

Analysis of gene expression changes during long-term induction of EMT in EpRas tumor cells by TGF-b1.

Project description:EMT is a developmental process, which can be reactivated in cancer cells. Cancer cells maintaining EMT in the circulation may have pro-metastatic properties. We used microarrays to profile EMT-related gene expression changes after 14 d of TGF-b1 treatment. EpRas cells were cultured in standard conditions either in the presence of absence of recombinant TGF-b1 (2 ng/ml) for 14 d. After this period, RNA was isolated from triplicate wells of treated and non-treated cells, and hybridized on Affymetrix microarrays.

2014-09-01 | E-GEOD-59922 | biostudies-arrayexpress

ChIP-seq analysis of the TGF-b1-treated intestinal organoids with or without Smad4 loss

Project description:The ChIP-seq analysis vilidated that Yap1/Smad2/3 signaling could regulate the transcriptional activity of key inflammasome genes upon TGF-b stimulation. In addition, TGF-b1 could be the downstream target gene of Yap. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for Yap1, Smad2/3 as well as the Tead1 in indicated intestinal organoids.

2024-06-01 | GSE229996 | 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