Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Generation of PDGFRα+ Cardioblasts from Pluripotent Stem Cells

ABSTRACT: We uncover a novel class of cardiac lineage cells, PDGFRα+Flk1- cardioblasts (PCB), from mouse and human pluripotent stem cells (PSC) using CsAYTE, a combination of small molecules – Cyclosporin A (CsA), ROCK inhibitor Y27362, antioxidant Trolox, and ALK5 inhibitor EW7197. To elucidate the genome-wide characteristics of PCB, microarray analysis was performed and compared with the spontaneously formed PCB, which were obtained without CsAYTE incubation (hereafter referred to as “sfPCB”), Flk1+ mesodermal precursor cells (MPC), and αMHC+ cardiomyocytes (M+CM)

ORGANISM(S): Mus musculus

PROVIDER: GSE65791 | GEO | 2017/02/10

SECONDARY ACCESSION(S): PRJNA275062

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Renal Cyclosporin-A (CsA) toxicity

Project description:The calcineurin inhibitor immunosuppressant cyclosporin A (CsA) soon gained clinical application, and became a standard of care in organ transplantation, as well as an important treatment option in a variety of autoimmune diseases. The immunosuppressive effect of CsA is mainly attributed to inhibiting calcineurin phosphatase activity, consequently favouring the inactive phosphorylated form of nuclear factor of activated T cells (NFAT). Renal toxicity is a serious adverse effect of CsA, but the underlying mechanisms are insufficiently understood. CsA has also been shown to induce episodic hypoxia (Fähling et al, 2017; doi: 10.1111/apha.12811). Here, we sought to identify molecular mechanisms of CsA nephrotoxicity.

2021-02-22 | GSE111516 | GEO

Renal Cyclosporin-A (CsA) toxicity

Project description:Renal Cyclosporin-A (CsA) toxicity

| PRJNA437288 | ENA

Murine Back Skin: Control vs. Cyclosporin A-treated

Project description:We analyzed the gene expression at the onset of hair growth induced by cyclosporin A (CsA), a well-known hair growth inducer, with DNA microarray, and unveiled the step-by-step progression of hair growth. KEYWORDS: Cyclosporin A, Cyclosporine A, Ciclosporin A

2009-12-24 | GSE16739 | GEO

Expression data of PDGFRα- and PDGFRα+ mesenchymal stem cells isolated from mouse periosteum

Project description:Expression data of PDGFRα- and PDGFRα+ mesenchymal stem cells isolated from mouse periosteum

| PRJNA644793 | ENA

Cyclosporin A inhibits prostate cancer growth through suppression of E2F8

Project description:Cyclosporin A (CsA) is a potent immunosuppressive agent used clinically in organ transplantation. In this study, we examined that CsA exerts anti-tumor activity against prostate cancer. We performed microarray experiments to investigate the effect of CsA on the transcriptome of prostate cancer cells. CsA potently induced transcriptome change and primarily affected cell cycle-related gene signatures. These results suggest that CsA can be used as a potential therapeutic agent or an intriguing tool for exploring prostate cancer biology and identifying novel therapeutic targets.

2023-10-04 | GSE109505 | GEO

Intronic polyadenylation of PDGFRα in stromal stem cells attenuates muscle fibrosis

Project description:The platelet-derived growth factor receptor alpha (PDGFRα) exhibits divergent effects in skeletal muscle. At physiological levels, signaling through this receptor promotes muscle development in growing embryos and proper angiogenesis in regenerating adult muscle. However, either increased PDGF ligands or enhanced PDGFRα pathway activity causes pathological fibrosis. This excessive collagen deposition, which is seen in aged and diseased muscle, interferes with proper muscle function and limits the effectiveness of gene- and cell-based therapies for muscle disorders. Although compelling evidence exists for the role of PDGFRα in fibrosis, little is known about the cells through which this pathway acts. Here we show that PDGFRα signaling regulates a population of muscle-resident fibro/adipogenic progenitors (FAPs) that play a supportive role in muscle regeneration but may also cause fibrosis when aberrantly regulated. We found that FAPs produce multiple transcriptional variants of PDGFRα with different polyadenylation sites, including an intronic variant that codes for a protein isoform containing a truncated kinase domain. This variant, upregulated during regeneration, acts as a decoy to inhibit PDGF signaling and to prevent FAP over-activation. Moreover, increasing expression of this isoform limits fibrosis in vivo, suggesting both biological relevance and therapeutic potential of modulating polyadenylation patterns in stem cell populations. We used microarrays to explore the biological effects of altering intronic polyadenylation of PDGFRα in FAPs in vivo.

2016-11-30 | GSE81744 | GEO

Intronic polyadenylation of PDGFRα in resident stem cells attenuates muscle fibrosis

2016-11-30 | GSE60099 | GEO

Expression data from 'naïve' and HVC-replicon containing Huh7 cells (Clone A cells)

Project description:Cyclophilin binding drugs, NIM811 and cyclosporin A (CsA), inhibit the replication of HCV replicon. We investigated the mode of action of these drugs and identified host factors essential for HCV replication in a subgenomic replicon model.

2009-05-03 | GSE15935 | GEO

Characterization of A Novel CRAC Inhibitor that Potently Blocks Human T cell Activation and Effector Functions

Project description:Store operated calcium entry (SOCE) downstream of T cell receptor (TCR) activation in T lymphocytes has been shown to be mediated mainly through the Calcium Release Activated Calcium (CRAC) channel. Here, we compared the effects of a novel, potent and selective CRAC inhibitor, 2,6-Difluoro-N-{5-[4-methyl-1-(5-methyl-thiazol-2-yl)-1,2,5,6-tetrahydro-pyridin-3-yl]-pyrazin-2-yl}-benzamide (RO2959), on T cell effector functions with that of a previously reported CRAC channel inhibitor, YM-58483, and a calcineurin inhibitor Cyclosporin A (CsA). Using both electrophysiological and calcium-based fluorescence measurements, we showed that RO2959 is a potent SOCE inhibitor that blocked an IP3-dependent current in CRAC-expressing RBL-2H3 cells and CHO cells stably expressing human Orai1 and Stim1, as well as SOCE in human primary CD4+ T cells triggered by either TCR stimulation or thapsigargin treatment. Furthermore, we demonstrated that RO2959 completely inhibited cytokine production as well as T cell proliferation mediated by TCR stimulation or MLR (Mixed Lymphocyte Reaction). Lastly, we showed by gene expression array analysis that RO2959 potently blocked TCR triggered gene expression and T cell functional pathways similar to CsA and FK506. Thus, both from a functional and transcriptional level, our data provide evidence that RO2959 is a novel and selective CRAC inhibitor that potently inhibits human T cell functions. PBMC from healthy donors (n=4) were stimulated with anti-CD3/CD28 in the presence or absence of CRAC inhibitor, CsA or FK506 for 24 hrs

2013-01-31 | E-GEOD-43210 | biostudies-arrayexpress

Tissue-resident PDGFRα stromal cells modulate both fibrosis and tissue revascularization during wound repair

Project description:PDGFRα+ cells are interstitial/perivascular mesenchymal progenitor cells that have been associated with fibro-adipogenic processes. However, their function during tissue homeostasis or in response to revascularization and regeneration stimuli remains to be fully defined. Here, by high-throughput transcriptomic analysis, adoptive transfer and multicolor lineage tracking we showed that PDGFRα+ cells from skeletal muscle cluster as a population that is transcriptionally distinct from other mesenchymal stromal cells and with an essential role in tissue revascularization and restructuring of ischemic areas. We further showed that tissue regeneration involves the removal of differentiated PDGFRα+-derived cells, while pathological healing occurred if PDGFRα+-derived cells persisted as terminally differentiated mesenchymal cells (e.g. myofibroblasts). From the perspective of tissue regeneration, these studies support a context-dependent 'yin-yang' biology of PDGFRα+ cells, that possess an innate ability to stabilize newly formed blood vessels and concurrently limit injury expansion after ischemia, while also being capable of promoting fibrosis in an unfavorable environment.

2019-07-01 | GSE101930 | 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