ArticleBlood2016
von Willebrand factor multimerization and the polarity of secretory pathways in endothelial cells.
Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
52 citing papers in PubMed, 111 citations in OpenAlex.
- Astragaloside IV confers vascular protection after traumatic brain injury through an Nrf2-dependent mechanism involving VWF.IBRO neuroscience reports · 2026Article
- Seventh Åland Island Meeting on von Willebrand Disease.Haemophilia : the official journal of the World Federation of Hemophilia · 2026Article
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- Rewriting the script: gene therapy and genome editing for von Willebrand Disease.Frontiers in genome editing · 2025Review
- Weibel-Palade bodies: function and role in thrombotic thrombocytopenic purpura and in diarrhea phase of STEC-hemolytic uremic syndrome.Pediatric nephrology (Berlin, Germany) · 2025Review
- Heparin Resistance in Patients Receiving Extracorporeal Membrane Oxygenation: A Review.Journal of clinical medicine · 2024Review
- Review
- Spatially targeted chemokine exocytosis guides transmigration at lymphatic endothelial multicellular junctions.The EMBO journal · 2024Article
- A defined clathrin-mediated trafficking pathway regulates sFLT1/VEGFR1 secretion from endothelial cells.Angiogenesis · 2024Article
- Clusterin knockdown has effects on intracellular and secreted von Willebrand factor in human umbilical vein endothelial cells.PloS one · 2024Article
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- A transcriptome analysis of basal and stimulated VWF release from endothelial cells derived from patients with type 1 VWD.Blood advances · 2023Article
- A defined clathrin-mediated trafficking pathway regulates sFLT1/VEGFR1 secretion from endothelial cells.bioRxiv : the preprint server for biology · 2023Article
- Article
- von Willebrand Factor: A Central Regulator of Arteriovenous Fistula Maturation Through Smooth Muscle Cell Proliferation and Outward Remodeling.Journal of the American Heart Association · 2022Article
- Defective VWF secretion due to expression of MYH9-RD E1841K mutant in endothelial cells disrupts hemostasis.Blood advances · 2022Article
- Syntaxin 5 determines Weibel-Palade body size and von Willebrand factor secretion by controlling Golgi architecture.Haematologica · 2022Article
- Ultra-Large Von Willebrand Factor and Platelets: Missing Links to the Pathogenesis of Aortic Valve Stenosis?JACC. Basic to translational science · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The von Willebrand factor (VWF) synthesized and secreted by endothelial cells is central to hemostasis and thrombosis, providing a multifunctional adhesive platform that brings together components needed for these processes. VWF secretion can occur from both apical and basolateral sides of endothelial cells, and from constitutive, basal, and regulated secretory pathways, the latter two via Weibel-Palade bodies (WPB). Although the amount and structure of VWF is crucial to its function, the extent of VWF release, multimerization, and polarity of the 3 secretory pathways have only been addressed separately, and with conflicting results. We set out to clarify these relationships using polarized human umbilical vein endothelial cells (HUVECs) grown on Transwell membranes. We found that regulated secretion of ultra-large (UL)-molecular-weight VWF predominantly occurred apically, consistent with a role in localized platelet capture in the vessel lumen. We found that constitutive secretion of low-molecular-weight (LMW) VWF is targeted basolaterally, toward the subendothelial matrix, using the adaptor protein complex 1 (AP-1), where it may provide the bulk of collagen-bound subendothelial VWF. We also found that basally-secreted VWF is composed of UL-VWF, released continuously from WPBs in the absence of stimuli, and occurs predominantly apically, suggesting this could be the main source of circulating plasma VWF. Together, we provide a unified dataset reporting the amount and multimeric state of VWF secreted from the constitutive, basal, and regulated pathways in polarized HUVECs, and have established a new role for AP-1 in the basolateral constitutive secretion of VWF.
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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.