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Endothelin-1 overexpression in mice increases vascular Vegfa164 and Vegfa188 alternative splice isoforms via enhanced Khdrbs3 expression

ABSTRACT: Transgenic mice with tamoxifen-inducible endothelium-restricted human endothelin-1 overexpression (ieET-1) exhibited blood pressure (BP) elevation after 3 weeks and 3 months induction. Vascular injury was observed only after a 3-month exposure to human ET-1 overexpression. It is unknown whether 3-week or 3-month exposure to ET-1 overexpression results in gene dysregulation. We aimed to identify differentially expressed (DE) microRNAs and total RNA in mesenteric arteries of ieET-1 mice after 3-week and 3-month induction of human ET-1 overexpression.

ORGANISM(S): Mus musculus

PROVIDER: GSE225866 | GEO | 2026/05/15

REPOSITORIES: GEO

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Endothelin-1 overexpression in mice increases vascular Vegfa164 and Vegfa188 alternative splice isoforms via enhanced Khdrbs3 expression

Project description:Transgenic mice with tamoxifen-inducible endothelium-restricted human endothelin-1 overexpression (ieET-1) exhibited blood pressure (BP) elevation after 3 weeks and 3 months induction. Vascular injury was observed only after a 3-month exposure to human ET-1 overexpression. It is unknown whether 3-week or 3-month exposure to ET-1 overexpression results in gene dysregulation. We aimed to identify differentially expressed (DE) microRNAs and total RNA in mesenteric arteries of ieET-1 mice after 3-week and 3-month induction of human ET-1 overexpression.

2026-05-15 | GSE225862 | GEO

Expression data from FAK null mouse embryonic fibroblasts treated with endothelin-1

Project description:Endothelin-1 (ET-1) plays a critical role in connective tissue remodeling by fibroblasts during tissue repair and fibrosis. We investigated the molecular pathways in the transmission of ET-1 signals that lead to features of connective tissue remodeling, in particular the role of FAK (focal adhesion kinase). We used microarrays to investigated whether FAK is required for ET-1 to promote the global programme of gene expression underlying myofibroblast formation and identified distinct classes of up-regulated genes during this process. Genes whose induction by ET-1 required FAK

2012-07-01 | GSE30356 | 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

Expression data from FAK null mouse embryonic fibroblasts treated with endothelin-1

2012-06-30 | E-GEOD-30356 | biostudies-arrayexpress

Nicotinamide counteracts endothelin-1’s detrimental effect on uterine decidualization during early pregnancy by influencing EDNRB

Project description:Endothelin-1 is involved in pathogenesis of preeclampsia. Mice (Edn1H/+) having excess endothelin-1developed preeclampsia-like phenotypes during pregnancy in a maternal genotype-dependent manner. Here, we investigate whether decidualization is impaired in Edn1H/+ dams, and whether nicotinamide (a potent inhibitor of endothelin-1) executes any beneficial effect. We compared implantation sites between wild type (WT) and Edn1H/+ dams with or without nicotinamide treatment. Implantation sites of Edn1H/+ dams exhibited abnormal ectoplacental cone and sinusoids with reduced vascular density in mesometrial regions of deciduae. There was more VEGF expression in decidua of Edn1H/+ dams than WT dams. The markers of decidualization were decreased in Edn1H/+ dams. Nicotinamide corrected the abnormality in Edn1H/+ dams. During differentiation (decidualization) of cultured human endometrial stomal cells, endothelin-1 halved the upregulated expression of markers of decidualization. Nicotinamide normalizes their expression. Nicotinamide counteracts ET-1’s detrimental effects on endometrial decidualization. It has potential to improve embryo implantation and subsequent pregnancy outcomes.

2025-12-04 | GSE306844 | GEO

Blockade of Endothelin Receptors Mitigates SARS-CoV-2-induced Osteochondral Damage

Project description:Previous studies have detected the presence of SARS-CoV-2 viral proteins in bronchial cartilage chondrocytes. We hypothesised that the leakage of viral proteins to local joint tissue was due to virus-induced endothelial dysfunction. Studies have also shown upregulation of endothelin-1 (ET-1), the most potent vasoconstrictor, in COVID patients. We are investigating the direct effect of SARS-CoV-2 spike protein (SP) and the host response to chondrocytes. Human mesenchymal stem cells (hMSCs)-differentiated chondrocytes were treated with either full-length SARS-CoV-2 spike protein (SP) only or a combination of spike protein, neutralising antibody to S1 and endothelin-1 (SAE) to mimic viral insult and host response respectively. RNA sequencing was performed to compared the change in transcriptome in control, SP and SAE. All samples were processed in the same batch. Default quality control parameters were used.

2024-05-08 | GSE267009 | GEO

Transcriptome analysis of Endothelin-3 or Neurotensin treated MuSCs

Project description:GPCRs have emerged as crucial regulators of muscle stem cell (MuSC) quiescence, yet the specific repertoire of GPCRs in quiescent MuSCs and the underlying regulatory network remain largely elusive. By employing pharmacological and inducible-genetic methods, we have identified two niche-derived GPCR ligands, endothelin-3 (ET-3) and neurotensin (NT), which bind to EDNRB and NTSR2 receptors, respectively, reinforcing the maintenance of MuSC quiescence. To comprehensively unravel the molecular mechanisms underlying the inhibitory effects of ET-3 and NT on MuSC activation, we conducted RNA sequencing (RNA-seq) analysis on FACS-purified MuSCs that underwent a 5-day in vitro treatment with ET-3 or NT

2024-07-25 | GSE234590 | GEO

Vascular gene expression in mice overexpressing human endothelin-1 targeted to the endothelium

Project description:Endothelin-1 (ET-1), an endothelium-derived vasoconstrictor peptide, plays a role in the pathophysiology of cardiovascular disease. Transgenic mice that overexpress human preproET-1 selectively in the endothelium (eET-1) exhibit endothelial dysfunction, hypertrophic remodeling and vascular inflammation of resistance-size arteries in the absence of blood pressure elevation. To understand the mechanisms whereby ET-1 induces vascular damage, vascular gene expression using DNA microarrays was employed. RNA from mesenteric arteries of female and male young (6-7 weeks) and mature (6-8 months) eET-1 and wild type (WT) mice was isolated and changes in gene expression were determined by genome-wide expression profiling using Illumina microarray. This study revealed a set of genes potentially regulated by ET-1, which might be implicated in ET-1 induced-vascular damage.

2010-09-01 | GSE19624 | GEO

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

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