ArticleResearch and practice in thrombosis and haemostasis2019
Alternative trafficking of Weibel-Palade body proteins in CRISPR/Cas9-engineered von Willebrand factor-deficient blood outgrowth endothelial cells.
Article in Research and practice in thrombosis and haemostasis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Allele-selective disruption of pathogenic VWF variants in type 2 von Willebrand disease using CRISPR/Cas9.Blood advances · 2026Article
- Role of Tie-2 Axis in Sepsis: A Potential Therapeutic Target.Journal of cellular and molecular medicine · 2025Review
- The future of siRNA-mediated approaches to treat von Willebrand disease.Expert review of hematology · 2025Review
- Chemigenetic Ca2+ indicators report elevated Ca2+ levels in endothelial Weibel-Palade bodies.PloS one · 2025Article
- Weibel-Palade bodies - secretory organelles at the interface of inflammation and hemostasis.Frontiers in cell and developmental biology · 2025Review
- Rewriting the script: gene therapy and genome editing for von Willebrand Disease.Frontiers in genome editing · 2025Review
- Angiopoietin-2 binds to multiple interactive sites within von Willebrand factor.Research and practice in thrombosis and haemostasis · 2023Article
- APOLD1 loss causes endothelial dysfunction involving cell junctions, cytoskeletal architecture, and Weibel-Palade bodies, while disrupting hemostasis.Haematologica · 2023Article
- Mutations in Neurobeachin-like 2 do not impact Weibel-Palade body biogenesis and von Willebrand factor secretion in gray platelet syndrome Endothelial Colony Forming Cells.Research and practice in thrombosis and haemostasis · 2023Article
- Automated segmentation and quantitative analysis of organelle morphology, localization and content using CellProfiler.PloS one · 2023Article
- Dispatch and delivery at the ER-Golgi interface: how endothelial cells tune their hemostatic response.The FEBS journal · 2022Article
- Syntaxin 5 determines Weibel-Palade body size and von Willebrand factor secretion by controlling Golgi architecture.Haematologica · 2022Article
- A Homozygous Deep Intronic Variant Causes Von Willebrand Factor Deficiency and Lack of Endothelial-Specific Secretory Organelles, Weibel-Palade Bodies.International journal of molecular sciences · 2022Article
- Multifaceted pathomolecular mechanism of a VWF large deletion involved in the pathogenesis of severe VWD.Blood advances · 2022Article
- Exploring Endothelial Colony-Forming Cells to Better Understand the Pathophysiology of Disease: An Updated Review.Stem cells international · 2022Review
- Quantitative 3D microscopy highlights altered von Willebrand factor α-granule storage in patients with von Willebrand disease with distinct pathogenic mechanisms.Research and practice in thrombosis and haemostasis · 2021Article
- Sec22b determines Weibel-Palade body length by controlling anterograde ER-Golgi transport.Haematologica · 2021Article
- Alternative trafficking of Weibel-Palade body proteins in CRISPR/Cas9-engineered von Willebrand factor-deficient blood outgrowth endothelial cells.Research and practice in thrombosis and haemostasis · 2019Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSynthesis of the hemostatic protein von Willebrand factor (VWF) drives formation of endothelial storage organelles called Weibel-Palade bodies (WPBs). In the absence of VWF, angiogenic and inflammatory mediators that are costored in WPBs are subject to alternative trafficking routes. In patients with von Willebrand disease (VWD), partial or complete absence of VWF/WPBs may lead to additional bleeding complications, such as angiodysplasia. Studies addressing the role of VWF using VWD patient-derived blood outgrowth endothelial cells (BOECs) have reported conflicting results due to the intrinsic heterogeneity of patient-derived BOECs.
objectiveTo generate a VWF-deficient endothelial cell model using clustered regularly interspaced short palindromic repeats (CRISPR) genome engineering of blood outgrowth endothelial cells.
methodsWe used CRISPR/CRISPR-associated protein 9 editing in single-donor cord blood-derived BOECs (cbBOECs) to generate clonal
resultsTwo
conclusionsCRISPR editing of
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.