ArticleResearch and practice in thrombosis and haemostasis2020
A rat model of severe VWD by elimination of the VWF gene using CRISPR/Cas9.
Article in Research and practice in thrombosis and haemostasis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Anatomical Identification and Pressure Myography of the Rat Middle Cerebral Artery: A Comprehensive Protocol for Diverse Genetic Models.bioRxiv : the preprint server for biology · 2026Article
- Loss of factor VIII in zebrafish rebalances antithrombin deficiency but has a limited bleeding diathesis.Blood advances · 2025Article
- The future of siRNA-mediated approaches to treat von Willebrand disease.Expert review of hematology · 2025Review
- Loss of factor VIII in zebrafish rebalances antithrombin deficiency but has a limited bleeding diathesis.bioRxiv : the preprint server for biology · 2024Article
- A novel mouse model of type 2N VWD was developed by CRISPR/Cas9 gene editing and recapitulates human type 2N VWD.Blood advances · 2022Article
- Advances in Genome Editing and Application to the Generation of Genetically Modified Rat Models.Frontiers in genetics · 2021Review
- A rat model of severe VWD by elimination of the VWF gene using CRISPR/Cas9.Research and practice in thrombosis and haemostasis · 2020Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundVon Willebrand Disease (VWD) is the most common inherited bleeding disorder, caused by quantitative and qualitative changes in von Willebrand factor (VWF). The biology of VWD, studied in canine, porcine, and murine models, differ in species-specific biology of VWF and the amenability to experimental manipulations such as phlebotomy. The factor VIII (FVIII) levels in these models are higher than in humans with type 3 VWD, suggesting functional differences between FVIII and VWF.ObjectivesTo develop a VWF knock out (VWF
methodsThe entire VWF gene was eliminated in Sprague-Dawley (Crl:SD) rats via CRISPR/Cas9-mediated gene editing. VWF antigen (VWF:Ag), VWF propeptide, and VWF collagen IV binding (VWF:CB4) levels were determined by ELISA assays and FVIII chromogenic activity (FVIII:C) levels by chromogenic FVIII assays. Lateral tail veins were transected to measure bleeding time. VWF
resultsBreeding of VWF ± rats yielded VWF
conclusionThis rat model of severe VWD due to elimination of the entire VWF gene recapitulates the severe secondary deficiency of FVIII seen in human type 3 VWD and facilitates the study of VWF and FVIII and their interactions.
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