ArticleKidney research and clinical practice2021
Modeling of endothelial cell dysfunction using human induced pluripotent stem cells derived from patients with end-stage renal disease.
Article in Kidney research and clinical practice, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Sources and applications of endothelial seed cells: a review.Stem cell research & therapy · 2024Review
- Sex in cardiovascular disease: Why this biological variable should be considered in in vitro models.Science advances · 2024Review
- Bioengineering Cell Therapy for Treatment of Peripheral Artery Disease.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Modeling ofCells · 2023Article
- Modeling of Fabry disease nephropathy using patient derived human induced pluripotent stem cells and kidney organoid system.Journal of translational medicine · 2023Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundEndothelial cell (EC) dysfunction is a frequent feature in patients with end-stage renal disease (ESRD). The aim of this study was to generate human induced pluripotent stem cells, differentiate ECs (hiPSC-ECs) from patients with ESRD, and appraise the usefulness of hiPSC-ECs as a model to investigate EC dysfunction.
methodsWe generated hiPSCs using peripheral blood mononuclear cells (PBMCs) isolated from three patients with ESRD and three healthy controls (HCs). Next, we differentiated hiPSC-ECs using the generated hiPSCs and assessed the expression of endothelial markers by immunofluorescence. The differentiation efficacy, EC dysfunction, and molecular signatures of EC-related genes based on microarray analysis were compared between the ESRD and HC groups.
resultsIn both groups, hiPSCs and hiPSC-ECs were successfully obtained based on induced pluripotent stem cell or EC marker expression in immunofluorescence and flow cytometry. However, the efficiency of differentiation of ECs from hiPSCs was lower in the ESRD-hiPSCs than in the HC-hiPSCs. In addition, unlike HC-hiPSC-ECs, ESRD-hiPSC-ECs failed to form interconnecting branching point networks in an in vitro tube formation assay. During microarray analysis, transcripts associated with oxidative stress and inflammation were upregulated and transcripts associated with vascular development and basement membrane extracellular matrix components were downregulated in ESRD-hiPSC-ECs relative to in HC-hiPSC-ECs.
conclusionESRD-hiPSC-ECs showed a greater level of EC dysfunction than HC-hiPSC-ECs did based on functional assay results and molecular profiles. hiPSC-ECs may be used as a disease model to investigate the pathophysiology of EC dysfunction in ESRD.
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