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Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human primary lung fibroblasts to investigate the effect of a 4 hour treatment of 100 nM endothelin-1

ABSTRACT: primary lung fibroblasts p3 from normal periphery of resected cancer. grown in DMEM 10% FBS, until confluence, then DMEM 0.5% FBS for 18 hours. Media were then changed and incubated for an additional 4 hours in the presence or absence of 100 nM endothelin-1. Data represent two independent experiments performed on two different occasions.

ORGANISM(S): Homo sapiens

SUBMITTER: Andrew Leask

PROVIDER: E-GEOD-1081 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Endothelin-1 induces expression of matrix-associated genes in lung fibroblasts through MEK/ERK.

Xu Shi-wen SW Howat Sarah L SL Renzoni Elisabetta A EA Holmes Alan A Pearson Jeremy D JD Dashwood Michael R MR Bou-Gharios George G Denton Christopher P CP du Bois Roland M RM Black Carol M CM Leask Andrew A Abraham David J DJ

The Journal of biological chemistry 20040323 22

The endothelins are a family of endothelium-derived peptides that possess a variety of biological activities, including potent vasoconstriction. Endothelin-1 (ET-1) is up-regulated during tissue repair and pulmonary fibrosis. Here, we use genome-wide expression array analysis to show that the addition of ET-1 (100 nm, 4 h) to normal lung fibroblasts directly induces expression of matrix and matrix-associated genes, including the profibrotic protein CCN2 (connective tissue growth factor, or CTGF) ...[more]

PMID: 15044479

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Effect of a 4 hour treatment of 100 nM endothelin-1 on human primary lung fibroblasts

Project description:primary lung fibroblasts p3 from normal periphery of resected cancer. grown in DMEM 10% FBS, until confluence, then DMEM 0.5% FBS for 18 hours. Media were then changed and incubated for an additional 4 hours in the presence or absence of 100 nM endothelin-1. Data represent two independent experiments performed on two different occasions. Keywords: other

2004-03-12 | GSE1081 | GEO

Endothelin-1 (ET-1) treated lung fibroblasts

Project description:Primary lung fibroblasts were grown to confluence in DMEM 10% FBS, serum starved in DMEM 0.5% FBS for 18 hours. Cells were then treated in the presence or absence of 100 nM ET-1 in the same medium for an additional 4 hours. Keywords: repeat sample

2004-02-28 | GSE981 | GEO

Transcription profiling of human endothelin treated lung fibroblasts

2008-06-16 | E-GEOD-981 | biostudies-arrayexpress

Phosphoproteomics of endothelin signalling

Project description:Time resolved phosphorylation changes were measured the melanoma cell lines A2058 and UACC257. An endothelin B receptor knockout of UACC257 was processed in parallel. Protein abundance was also compared at the latest time point of the study (90 min) using DIA-SWATH

2019-10-09 | PXD012316 | Pride

Endothelin signaling activates neural crest gene expression via a MEF2C-dependent positive-feedback transcriptional mechanism

Project description:Endothelin signaling is one of the essential signaling pathways that control vertebrate development. Dysregulated Endothelin signaling plays an important role in the pathogenesis of human diseases such as Hirschsprung’s disease, pulmonary hypertension and cancer. However, the downstream transcriptional program and transcriptional factors of Endothelin signaling have been incompletely understood. Here, we used RNA-sequencing to identify the genes regulated by Endothelin signaling in the neural crest, where Endothelin signaling functions primarily during development. We further demonstrate that Endothelin induces gene expression through the de-repression of the MADS Box transcription factor MEF2C. Moreover, in the Mef2c gene locus, we identified an Endothelin responsive cis-regulatory element which functions as a central component of an Endothelin-MEF2C positive feedback transcriptional mechanism that regulates downstream gene expression.

2016-11-15 | GSE47919 | GEO

Fibroblast secretome proteomic analysis

Project description:LV fibroblasts were isolated from control (day 0), and infarcted regions at day 1, day 3, and day 7 after myocardial infarction (MI). Cells were isolated in DMEM in 10% fetal bovine serum and were seeded into 6-well plates and were allowed to grow to 80% confluence in DMEM supplemented with 10% fetal bovine serum (FBS). Cells were serum starved (DMEM + 0.1% FBS) for 18 h and then media was changed and secretome was collected after 24 h. The sample sizes are n=3 biological replicates for each time point.

2019-10-25 | PXD011778 | Pride

RNAPolII CUT&Tag profiles of MDA-MB-231 cell line with repression of CDK genes and PRMT5

Project description:A clonal doxycycline inducible dCas9-KRAB MDA-MB-231 cell line to control repression of CDK genes and PRMT5. On day 1 of the experiment cells were infected with lentiviruses containing the appropriate targeting/NTC sgRNAs driven by the human U6 promoter at an MOI of ~3 for each virus to ensure all cells were transduced. Cells were transduced in DMEM + 10% FBS with the addition of 8 μg/mL polybrene. 16 hours after the time of transduction, media was changed to DMEM +10% FBS. 24 hours after this, the cell culture media was switched to DMEM + 10%FBS containing 2μg/mL puromycin to ensure no uninfected cells remain. 48 hours after this, cell culture media was changed to DMEM + 10%FBS containing 2 μg/mL puromycin and 1 μg/mL doxycycline to induce dCas9-KRAB expression. 48 hours after this, cells were processed for CUT&Tag library prep following the manufacturer's recommendations.

2023-05-01 | GSE227432 | GEO

Endothelin-1-Endothelin B complex contributes to oligodendrocyte differentiation and myelin deficits during preterm white matter injury

Project description:Preterm cerebral white matter injury (WMI), a major form of prenatal brain injury, may potentially be treated by oligodendrocyte (OL) precursor cell (OPC) transplantation. However, the defective differentiation of OPCs during WMI seriously hampers the clinical application of OPC transplantation. Thus, improving the ability of transplanted OPCs to differentiate is critical to OPC transplantation therapy for WMI. Here, we established a hypoxia-ischemia-induced preterm WMI model in mice and screened the molecules affected by WMI using single-cell RNA sequencing. We revealed that endothelin (ET)-1 and endothelin receptor B (ETB) were a pair of signaling molecules for the interaction between neurons and OPCs, and that preterm WMI led to an increase in the number of ETB-positive OPCs and premyelinating OLs. Furthermore, the maturation of OLs was reduced by knocking out ETB, but promoted by stimulating ET-1/ETB signaling. Our work reveals a new signaling module for neuron-OPC interaction and provides new insight for therapy targeting preterm WMI.

2023-03-04 | GSE225580 | GEO

Progenitor-derived endothelin controls dermal sheath contraction for hair follicle regression

Project description:Progenitor cell death and dermal papilla relocation during the regression phase of the hair growth cycle are essential for stem cell activation and follicle regeneration. This drastic follicle remodeling is coordinated by dermal sheath (DS) smooth muscle contraction, but how DS-generated forces are regulated is unknown. Here, we identify endothelin signaling - a potent vasoconstriction-regulating pathway - as the key activating mechanism of DS contraction. Pharmacological blocking or genetic ablation of both endothelin receptors, ETA and ETB, impedes DS contraction and halts follicle regression. Progenitors at the epithelial strand bottleneck are the main source of endothelin ligand ET-1, which is required for follicle regression. ET signaling in DS cells and downstream contraction is dynamically regulated by cytoplasmic Ca2+ levels via cell membrane and sarcoplasmic reticulum calcium channels. Together, these findings illuminate an epithelial-mesenchymal-interaction paradigm in which progenitors - before undergoing programmed cell death - control the contraction of the surrounding sheath smooth muscle to orchestrate homeostatic tissue regression and follicle reorganization.

2022-10-31 | GSE215133 | GEO

Cardiac Metabolic Deregulation Induced by the Tyrosine Kinase Receptor Inhibitor Sunitinib is rescued by Endothelin Receptor Antagonism

Project description:The growing field of cardio-oncology addresses the side effects of cancer treatment on the cardiovascular system. Here, we explored the cardiotoxicity of the antiangiogenic therapy, sunitinib, in the mouse heart from a diagnostic and therapeutic perspective. We showed that sunitinib induces an anaerobic switch of cellular metabolism within the myocardium which is associated with the development of myocardial fibrosis and reduced left ventricular ejection fraction as demonstrated by echocardiography. The capacity of positron emission tomography with [18F]fluorodeoxyglucose to detect the changes in cardiac metabolism caused by sunitinib was dependent on fasting status and duration of treatment. Pan proteomic analysis in the myocardium showed that sunitinib induced (i) an early metabolic switch with enhanced glycolysis and reduced oxidative phosphorylation, and (ii) a metabolic failure to use glucose as energy substrate, similar to the insulin resistance found in type 2 diabetes. Co-administration of macitentan, the endothelin receptor antagonist, to sunitinib-treated animals prevented both metabolic defects, restored glucose uptake and cardiac function, and prevented myocardial fibrosis. These results support the endothelin system in mediating the cardiotoxic effects of sunitinib and endothelin receptor antagonism as a potential therapeutic approach to prevent cardiotoxicity. Furthermore, metabolic and functional imaging can monitor the cardiotoxic effects and the benefits of endothelin antagonism in a theranostic approach.

2017-07-14 | PXD006888 | Pride

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