Tanscriptional profile of primary endothelial cells (HUVEC) in ADA2 depleted setting and effect of Dipyridamole (DPM) treatment
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ABSTRACT: Adenosine deaminase 2 deficiency (DADA2) is an inherited disorder which can cause vasculitis of medium-sized blood vessels. The disease is caused by mutations in the CECR1 gene, which encodes a key metabolic enzyme in the purine pathway. It is not clear how DADA2 leads to vasculitis, and there are currently limited treatment options. We, therefore, as a first step aimed to study the altered gene expression profile of primary endothelial cells in ADA2 depleted setting and then assessed the effect of Dipyridamole (DPM), a pharmacological inhibitor of ENT- transporters, on the differentially expressed genes. The whole genome transcriptome analysis revealed a robust induction of an IFNβ-stimulated gene signature in unstimulated siADA2-treated cells. Differentially expressed transcripts in this dataset included genes encoding pro-inflammatory cytokines, chemokines, and innate immune response proteins. Pre-treatment with dipyridamole (DPM), reduced expression of the IFNβ-driven gene signature upon depletion of ADA2.
ORGANISM(S): Homo sapiens
PROVIDER: GSE150540 | GEO | 2020/06/01
REPOSITORIES: GEO
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