ArticleBritish journal of haematology2023
Sickle red blood cell-derived extracellular vesicles activate endothelial cells and enhance sickle red cell adhesion mediated by von Willebrand factor.
Article in British journal of haematology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- Shear-Activated von Willebrand Factor Captures Extracellular Vesicles to Promote Platelet Activation and Metastasis.Journal of extracellular vesicles · 2026Article
- Mouse models to study von Willebrand factor in inflammation: a scoping review.Intensive care medicine experimental · 2026Review
- Microfluidics for Blood Disorders and Hematological Disease Monitoring and Modeling.International journal of molecular sciences · 2026Review
- Advancing Extracellular Vesicle Research: A Review of Systems Biology and Multiomics Perspectives.Proteomics · 2026Review
- Abnormalities of hemostasis in sickle cell patients and predisposition to thrombotic risk: a systematic review and meta-analysis.Thrombosis journal · 2025Review
- Emerging pathways in thromboinflammation of sickle cell disease: novel findings in disease pathogenesis.Research and practice in thrombosis and haemostasis · 2025Review
- Extracellular vesicles modulate endothelial nitric oxide production in patients with β‑thalassaemia/HbE.Biomedical reports · 2025Article
- Crosstalk Between Sickle Cell Disease and Ferroptosis.International journal of molecular sciences · 2025Review
- Initiation of Progressive Morphological Transition Towards an Echino-Stomato-Spherocytic Phenotype by Phosphatidylserine Externalization and Its Implication in Thrombosis.International journal of molecular sciences · 2025Article
- Adverse clinical outcomes associated with sickle cell trait at high altitude.Haematologica · 2025Article
- Red blood cell extracellular vesicles: new frontiers in hematological biomarker discovery.Frontiers in medicine · 2025Review
- Vascularized platforms for investigating cell communication via extracellular vesicles.Biomicrofluidics · 2024Review
- Motion blur microscopy: in vitro imaging of cell adhesion dynamics in whole blood flow.Nature communications · 2024Article
- Motion Blur Microscopy.bioRxiv : the preprint server for biology · 2024Article
- An update on recent studies of extracellular vesicles and their role in hypercoagulability in thalassemia (Review).Biomedical reports · 2024Review
- Autophagy Behavior in Endothelial Cell Regeneration.Current aging science · 2024Review
- Heme (dys)homeostasis and liver disease.Frontiers in physiology · 2024Review
- Red Blood Cell-Derived Extracellular Vesicles: An Overview of Current Research Progress, Challenges, and Opportunities.Biomedicines · 2023Review
- Executive Function and Processing Speed in Children Living with Sickle Cell Anemia.Children (Basel, Switzerland) · 2023Article
- Not All Heme is "Free" in Sickle Cell Disease.HemaSphere · 2023Article
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
Abstract
Endothelial activation and sickle red blood cell (RBC) adhesion are central to the pathogenesis of sickle cell disease (SCD). Quantitatively, RBC-derived extracellular vesicles (REVs) are more abundant from SS RBCs compared with healthy RBCs (AA RBCs). Sickle RBC-derived REVs (SS REVs) are known to promote endothelial cell (EC) activation through cell signalling and transcriptional regulation at longer terms. However, the SS REV-mediated short-term non-transcriptional response of EC is unclear. Here, we examined the impact of SS REVs on acute microvascular EC activation and RBC adhesion at 2 h. Compared with AA REVs, SS REVs promoted human pulmonary microvascular ECs (HPMEC) activation indicated by increased von Willebrand factor (VWF) expression. Under microfluidic conditions, we found abnormal SS RBC adhesion to HPMECs exposed to SS REVs. This enhanced SS RBC adhesion was reduced by haeme binding protein haemopexin or VWF cleaving protease ADAMTS13 to a level similar to HPMECs treated with AA REVs. Consistent with these observations, haemin- or SS REV-induced microvascular stasis in SS mice with implanted dorsal skin-fold chambers that was inhibited by ADAMTS13. The adhesion induced by SS REVs was variable and was higher with SS RBCs from patients with increased markers of haemolysis (lactate dehydrogenase and reticulocyte count) or a concomitant clinical diagnosis of deep vein thrombosis. Our results emphasise the critical contribution made by REVs to the pathophysiology of SCD by triggering acute microvascular EC activation and abnormal RBC adhesion. These findings may help to better understand acute pathophysiological mechanism of SCD and thereby the development of new treatment strategies using VWF as a potential target.
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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 Socratic graph.