Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE143482 | GEO | 2020/08/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

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

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

| PRJNA600741 | 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

Effects of IL-13 on primary esophageal fibroblasts

Project description:This is part of a larger experiment in which the effects of IL-13, LIGHT and TGF-B1 on human primary esophageal fibroblasts were analyzed and compared.

2022-09-29 | GSE212731 | GEO

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

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

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

Project description: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.

2019-04-02 | GSE129164 | GEO

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

2014-09-01 | GSE59922 | GEO

Genes expression of cervical squamous cell carcinoma, CaSki cells, treated with or without recombinant TGF-b1 (2 ng/mL)

Project description:Aggressive local invasion is the major way of spread in uterine cervical squamous cell carcinoma (CSCC). Although TGF-b facilitates invasion of various types of cancer cells, the role of TGF-b pathway in CSCC is unclear. Through array-based analysis, immunohistochemical staining of human endometrial cancer tissue, it is shown that interaction between CSCC cells and surrounding cancer asscocited fibroblasts (CAFs) activates TGF-b via TSP-1 secretion to facilitate CSCC invade, resulting in up-regulation of pSMAD3 in CSCC cells to promote invasion. These results suggest that activation of TGF-b induced by the interaction between CSCC cells and CAFs could play a key role in the initiation of tumor spreads. We used microarrays to clarify the changes of gene expression along with recombinant TGF-b1 treatment and to confirm whether there are any changes on genes expression related to TGF-b pathway.

2014-05-09 | E-GEOD-57441 | biostudies-arrayexpress

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