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RNAseq of DHX15-silenced endothelial cells

ABSTRACT: RNAseq of DHX15-silenced endothelial cells

PROVIDER: PRJNA759857 | ENA |

REPOSITORIES: ENA

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RNAseq of DHX15-silenced endothelial cells

Project description:We performed RNAseq in immortalized mouse-liver sinusoidal endothelial cells with or without DHX15 gene silencing. The RNA-seq experiment allowed us to generate 122,968 paired-end reads that were successfully mapped to the mouse reference GRCm38 genome assembly. After quality control analysis, four samples per experimental condition were included in the analysis.

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Endothelial dysfunction in NR2F2-silenced cells - human lung microvascular endothelial cells model

Project description:Orphan nuclear receptor chicken ovalbumin upstream promoter transcription factor 2 (COUPTF2; NR2F2) is highly expressed in endothelial cells (ECs) and Nr2f2 knockout produces lethal cardiovascular defects. In humans, NR2F2 mutations result in both congenital heart disease and diaphragmatic hernia, conditions associated with the development of pulmonary arterial hypertension (PAH). However, COUPTF2 functions in mature endothelium are uncertain. NR2F2 knockdown in primary human endothelial cells (ECs) led to an interferon-biased inflammatory response, endothelial-to-mesenchymal transition, proliferation, hypermigration, apoptosis-resistance and mitochondrial dysfunction. These phenotypic changes were associated with AKT activation and increased Dickkopf-1 (DKK1) expression, a Wnt/β-catenin pathway inhibitor. DKK1 was also elevated in patients with PAH and secreted in response to loss of bone morphogenetic receptor type 2 (BMPR2), the archetypal PAH-associated genetic defect. Together, these findings demonstrate that endothelial NR2F2 suppresses inflammation and proliferation. Thus, NR2F2 loss disrupts EC homeostasis and may promote pathologic vascular remodeling in the development of PAH.

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Endothelial dysfunction in NR2F2-silenced cells - human coronary artery endothelial cells model

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Loss of ERG in human lung endothelial cells leads to release of pro-inflammatory and pro-fibrotic factors.

Project description:: Although vascular dysfunction is a hallmark of chronic aging-associated diseases, including idiopathic pulmonary fibrosis, the role of the pulmonary vasculature to lung repair versus lung fibrosis is not fully understood. We identified the endothelial transcription factor ETS-related gene (ERG) as an orchestrator of vascular homeostasis and repair following lung injury. To evaluate whether loss of endothelial ERG influences the activation of neighboring naïve lung fibroblasts, we collected the conditioned media (CM) generated by control- and ERG-silenced human lung endothelial cells (ECs) and we applied them to normal human lung fibroblasts. We found that CM from ERG-silenced human lung ECs strongly promoted human lung fibroblast activation and enhanced the effect of the fibrogenic mediator TGF. In support of these results, analysis of CM using nanoscale liquid chromatography coupled to tandem mass spectrometry (nano LC-MS/MS) revealed increased secretion of numerous pro-inflammatory and pro-fibrogenic mediators by ERG-silenced human lung ECs in comparison to control-silenced human lung ECs.

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