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Article ; Online: The contribution of the sinusoidal endothelial cell receptors CLEC4M, stabilin-2, and SCARA5 to VWF-FVIII clearance in thrombosis and hemostasis.

Swystun, Laura L / Michels, Alison / Lillicrap, David

Journal of thrombosis and haemostasis : JTH

2023 Volume 21, Issue 8, Page(s) 2007–2019

Abstract: Quantitative abnormalities in factor VIII (FVIII) and its binding partner, von Willebrand factor (VWF), are associated with an increased risk of bleeding or thrombosis, and pathways that regulate the clearance of VWF-FVIII can strongly influence their ... ...

Abstract	Quantitative abnormalities in factor VIII (FVIII) and its binding partner, von Willebrand factor (VWF), are associated with an increased risk of bleeding or thrombosis, and pathways that regulate the clearance of VWF-FVIII can strongly influence their plasma levels. In 2010, the Cohorts for Heart and Aging Research in Genome Epidemiology (CHARGE) on genome-wide association study meta-analysis identified variants in the genes for the sinusoidal endothelial receptors C-type lectin domain family 4 member M (CLEC4M), stabilin-2, and scavenger receptor class A member 5 (SCARA5) as being associated with plasma levels of VWF and/or FVIII in normal individuals. The ability of these receptors to bind, internalize, and clear the VWF-FVIII complex from the circulation has now been reported in a series of studies using in vitro and in vivo models. The receptor stabilin-2 has also been shown to modulate the immune response to infused VWF-FVIII concentrates in a murine model. In addition, the influence of genetic variants in CLEC4M, STAB2, and SCARA5 on type 1 von Willebrand disease/low VWF phenotype, FVIII pharmacokinetics, and the risk of venous thromboembolism has been described in a number of patient-based studies. Understanding the role of these receptors in the regulation of VWF-FVIII clearance has led to significant insights into the genomic architecture that modulates plasma VWF and FVIII levels, improving the understanding of pathways that regulate VWF-FVIII clearance and the mechanistic basis of quantitative VWF-FVIII pathologies.
MeSH term(s)	Animals ; Mice ; von Willebrand Factor/metabolism ; Genome-Wide Association Study ; Factor VIII/genetics ; Hemostasis/genetics ; Thrombosis/genetics ; Thrombosis/metabolism ; Endothelial Cells/metabolism ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/metabolism ; Hemostatics ; von Willebrand Diseases/metabolism ; Scavenger Receptors, Class A/genetics
Chemical Substances	von Willebrand Factor ; Factor VIII (9001-27-8) ; Receptors, Cell Surface ; Hemostatics ; SCARA5 protein, mouse ; Scavenger Receptors, Class A
Language	English
Publishing date	2023-04-19
Publishing country	England
Document type	Meta-Analysis ; Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1016/j.jtha.2023.04.014
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Article ; Online: Role of von Willebrand factor in venous thromboembolic disease.

Michels, Alison / Lillicrap, David / Yacob, Michael

JVS-vascular science

2021 Volume 3, Page(s) 17–29

Abstract: Objective: Evolving evidence of the shared risk factors and pathogenic mechanisms in arterial and venous thrombosis questions of the strict vascular dichotomy of arterial vs venous. The connection between arterial and venous thrombosis has been ... ...

Abstract	Objective: Evolving evidence of the shared risk factors and pathogenic mechanisms in arterial and venous thrombosis questions of the strict vascular dichotomy of arterial vs venous. The connection between arterial and venous thrombosis has been highlighted by common underlying inflammatory processes, a concept known as thromboinflammatory disease. Using this relationship, we can apply knowledge from arterial disease to better understand and potentially mitigate venous disease. A protein that has been extensively studied in atherothrombotic disease and inflammation is von Willebrand factor (VWF). Because many predisposing and provoking factors of venous thromboembolism (VTE) have been shown to directly modulate VWF levels, it is, perhaps, not surprising that VWF has been highlighted by several recent association studies of patients with VTE. Methods: In the present narrative review, we investigated more deeply the effects of VWF in venous disease by synthesizing the data from clinical studies of deep vein thrombosis of the limbs, pulmonary embolism, portal and cerebral vein thrombosis, and the complications of thrombosis, including post-thrombotic syndrome, venous insufficiency, and chronic thromboembolic pulmonary hypertension. We have also discussed the findings from preclinical studies to highlight novel VWF biochemistry in thrombosis and therapeutics. Results: Across the spectrum of venous thromboembolic disease, we consistently observed that elevated VWF levels conferred an increased risk of VTE and long-term venous complications. We have highlighted important findings from VWF molecular research and have proposed mechanisms by which VWF participates in venous disease. Emerging evidence from preclinical studies might reveal novel targets for thromboinflammatory disease, including specific VWF pathophysiology. Furthermore, we have highlighted the utility of measuring VWF to prognosticate and risk stratify for VTE and its complications. Conclusions: As the prevalence of inflammatory processes, such as aging, obesity, and diabetes increases in our population, it is critical to understand the evolving role of VWF in venous disease to guide clinical decisions and therapeutics.
Language	English
Publishing date	2021-10-07
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2666-3503
ISSN (online)	2666-3503
DOI	10.1016/j.jvssci.2021.08.002
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Article ; Online: Stabilin-2 deficiency increases thrombotic burden and alters the composition of venous thrombi in a mouse model.

Michels, Alison / Swystun, Laura L / Dwyer, Courtney N / Rawley, Orla / Nesbitt, Kate / Notley, Colleen / Lillicrap, David

Journal of thrombosis and haemostasis : JTH

2021 Volume 19, Issue 10, Page(s) 2440–2453

Abstract: Background: Stabilin-2 is an endocytic scavenger receptor that mediates the clearance of glycosaminoglycans, phosphatidylserine-expressing cells, and the von Willebrand factor-factor VIII (FVIII) complex. In a genome-wide screening study, pathogenic ... ...

Abstract	Background: Stabilin-2 is an endocytic scavenger receptor that mediates the clearance of glycosaminoglycans, phosphatidylserine-expressing cells, and the von Willebrand factor-factor VIII (FVIII) complex. In a genome-wide screening study, pathogenic loss-of-function variants in the human STAB2 gene associated with an increased incidence of unprovoked venous thromboembolism (VTE). However, the specific mechanism(s) by which stabilin-2 deficiency influences the pathogenesis of VTE is unknown. Objectives: The aim of this study was to assess the influence of stabilin-2 on deep vein thrombosis (DVT) and to characterize the underlying prothrombotic phenotype of stabilin-2 deficiency in a mouse model. Methods: DVT was induced using the inferior vena cava (IVC) stenosis model in two independent cohorts (littermates and non-littermates) of wild-type (Stab2 Results: Incidence of thrombus formation was not altered between Stab2 Conclusions: These data suggest that stabilin-2 deficiency associates with a prothrombotic phenotype involving elevated levels of neutrophil extracellular trap-releasing leukocytes coupled with endogenous procoagulant activity, resulting in larger and qualitatively distinct venous thrombi.
MeSH term(s)	Animals ; Cell Adhesion Molecules, Neuronal ; Disease Models, Animal ; Extracellular Traps ; Mice ; Mice, Knockout ; Thrombosis ; Veins ; von Willebrand Factor
Chemical Substances	Cell Adhesion Molecules, Neuronal ; Stab2 protein, mouse ; von Willebrand Factor
Language	English
Publishing date	2021-07-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1111/jth.15429
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Article ; Online: The mechanistic and structural role of von Willebrand factor in endotoxemia-enhanced deep vein thrombosis in mice.

Choi, Seon Jae / Dwyer, Courtney N / Rapkin, Lindsy / Cormier, Matthew / Hindmarch, Charles C T / Nesbitt, Kate / Michels, Alison / Hopman, Wilma / Swystun, Laura L / Lillicrap, David

Journal of thrombosis and haemostasis : JTH

2022 Volume 21, Issue 3, Page(s) 586–598

Abstract: Background: Although the concept of immunothrombosis has established a link between inflammation and thrombosis, the role of inflammation in the pathogenesis of deep vein thrombosis remains to be fully elucidated. Further, although various constituents ... ...

Abstract	Background: Although the concept of immunothrombosis has established a link between inflammation and thrombosis, the role of inflammation in the pathogenesis of deep vein thrombosis remains to be fully elucidated. Further, although various constituents of venous thrombi have been identified, their localizations and cellular and molecular interactions are yet to be combined in a single, multiplexed analysis. Objectives: The objective of this study was to investigate the role of the von Willebrand factor (VWF) in inflammation-associated venous thrombosis. We also performed a proof-of-concept study of imaging mass cytometry to quantitatively and simultaneously analyze the localizations and interactions of 10 venous thrombus constituents. Methods: We combined the murine inferior vena cava stenosis model of deep vein thrombosis with the lipopolysaccharide model of endotoxemia. We also performed a proof-of-concept study of imaging mass cytometry to assess the feasibility of this approach in analyzing the structural composition of thrombi. Results: We found that lipopolysaccharide-treated mice had significantly higher incidences of venous thrombosis, an effect that was mitigated when VWF was inhibited using inhibitory αVWF antibodies. Our detailed structural analysis also showed that most thrombus components are localized in the white thrombus regardless of endotoxemia. Moreover, although endotoxemia modulated the relative representation and interactions of VWF with other thrombus constituents, the scaffolding network, comprised VWF, fibrin, and neutrophil extracellular traps, remained largely unaffected. Conclusions: We observe a key role for VWF in the pathogenesis of inflammation-associated venous thrombosis while providing a more comprehensive insight into the molecular interactions that constitute the architecture of venous thrombi.
MeSH term(s)	Mice ; Animals ; von Willebrand Factor ; Endotoxemia ; Lipopolysaccharides ; Venous Thrombosis/etiology ; Thrombosis/complications
Chemical Substances	von Willebrand Factor ; Lipopolysaccharides
Language	English
Publishing date	2022-12-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1016/j.jtha.2022.11.022
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Article ; Online: von Willebrand Factor Is a Critical Mediator of Deep Vein Thrombosis in a Mouse Model of Diet-Induced Obesity.

Michels, Alison / Dwyer, Courtney N / Mewburn, Jeffrey / Nesbitt, Kate / Kawecki, Charlotte / Lenting, Peter / Swystun, Laura L / Lillicrap, David

Arteriosclerosis, thrombosis, and vascular biology

2020 Volume 40, Issue 12, Page(s) 2860–2874

Abstract: Objective: Obesity is characterized by chronic low-grade inflammation and consequentially a hypercoagulable state, associating with an increased incidence of venous thromboembolism. Increased VWF (von Willebrand factor) plasma concentration and ... ...

Abstract	Objective: Obesity is characterized by chronic low-grade inflammation and consequentially a hypercoagulable state, associating with an increased incidence of venous thromboembolism. Increased VWF (von Willebrand factor) plasma concentration and procoagulant function are independent risk factors for venous thromboembolism and are elevated in obese patients. Here, we explore the pathobiological role of VWF in obesity-associated venous thrombosis using murine models. Approach and Results: We first showed that diet-induced obese mice have increased VWF plasma levels and FVIII (factor VIII) activity compared with littermate controls. Elevated VWF levels appeared to be because of both increased synthesis and impaired clearance. Diet-induced obesity-associated venous thrombosis was assessed using the inferior vena cava-stenosis model of deep vein thrombosis. Diet-induced obese mice developed larger venous thrombi that were rich in VWF, erythrocytes, and leukocytes. Administering a polyclonal anti-VWF antibody or an anti-VWF A1 domain nanobody was protective against obesity-mediated thrombogenicity. Delayed administration (3 hours post-inferior vena cava stenosis) similarly reduced thrombus weight in diet-induced obese mice. Conclusions: This study demonstrates the critical role of VWF in the complex, thrombo-inflammatory state of obesity. It adds to the growing rationale for targeting VWF-specific interactions in thrombotic disease.
MeSH term(s)	ADAMTS13 Protein/genetics ; ADAMTS13 Protein/metabolism ; Animals ; Diet, High-Fat ; Disease Models, Animal ; Female ; Fibrinolytic Agents/pharmacology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Obesity/complications ; Obesity/metabolism ; Signal Transduction ; Single-Domain Antibodies/pharmacology ; Vena Cava, Inferior/drug effects ; Vena Cava, Inferior/metabolism ; Vena Cava, Inferior/pathology ; Venous Thrombosis/etiology ; Venous Thrombosis/metabolism ; Venous Thrombosis/pathology ; Venous Thrombosis/prevention & control ; von Willebrand Factor/antagonists & inhibitors ; von Willebrand Factor/genetics ; von Willebrand Factor/metabolism
Chemical Substances	Fibrinolytic Agents ; Single-Domain Antibodies ; von Willebrand Factor ; ADAMTS13 protein, mouse (EC 3.4.24.-) ; ADAMTS13 Protein (EC 3.4.24.87)
Language	English
Publishing date	2020-09-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.120.314690
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Article: Investigating von willebrand factor pathophysiology using a flow chamber model of von willebrand factor-platelet string formation

Michels, Alison / Swystun, Laura L / Mewburn, Jeffrey / Albánez, Silvia / Lillicrap, David

Journal of visualized experiments. 2017 Aug. 14, , no. 126

2017

Abstract: Von Willebrand factor (VWF) is a multimeric glycoprotein coagulation factor that mediates platelet adhesion and aggregation at sites of endothelial damage and that carries factor VIII in the circulation. VWF is synthesized by endothelial cells and is ... ...

Abstract	Von Willebrand factor (VWF) is a multimeric glycoprotein coagulation factor that mediates platelet adhesion and aggregation at sites of endothelial damage and that carries factor VIII in the circulation. VWF is synthesized by endothelial cells and is either released constitutively into the plasma or is stored in specialized organelles, called Weibel-Palade bodies (WPBs), for on-demand release in response to hemostatic challenge. Procoagulant and proinflammatory stimuli can rapidly induce WPB exocytosis and VWF release. The majority of VWF released by endothelial cells circulates in the plasma; however, a proportion of VWF is anchored to the endothelial cell surface. Under conditions of physiological shear, endothelial-anchored VWF can bind to platelets, forming a VWF-platelet string that may represent the nidus of thrombus formation. A flow chamber system can be used to visually observe the release of VWF from endothelial cells and the subsequent platelet capture in a manner that is reproducible and relevant to the pathophysiology of VWF-mediated thrombus formation. Using this methodology, endothelial cells are cultured in a flow chamber and are subsequently stimulated with secretagogues to induce WPB exocytosis. Washed platelets are then perfused over the activated endothelium. The platelets are activated and subsequently bind to elongated VWF strings in the direction of fluid flow. Using extracellular histones as a procoagulant and proinflammatory stimulus, we observed increased VWF-platelet string formation on histone-treated endothelial cells compared to untreated endothelial cells. This protocol describes a quantitative, visual, and real-time assessment of the activation of VWF-platelet interactions in models of thrombosis and hemostasis.
Keywords	adhesion ; blood platelets ; cell adhesion ; coagulation ; endothelial cells ; endothelium ; exocytosis ; factor VIII ; glycoproteins ; hemostasis ; histones ; models ; organelles ; pathophysiology ; thrombosis
Language	English
Dates of publication	2017-0814
Size	p. e55917.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/55917
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation.

Michels, Alison / Swystun, Laura L / Mewburn, Jeffrey / Albánez, Silvia / Lillicrap, David

Journal of visualized experiments : JoVE

2017 , Issue 126

Abstract	Von Willebrand factor (VWF) is a multimeric glycoprotein coagulation factor that mediates platelet adhesion and aggregation at sites of endothelial damage and that carries factor VIII in the circulation. VWF is synthesized by endothelial cells and is either released constitutively into the plasma or is stored in specialized organelles, called Weibel-Palade bodies (WPBs), for on-demand release in response to hemostatic challenge. Procoagulant and proinflammatory stimuli can rapidly induce WPB exocytosis and VWF release. The majority of VWF released by endothelial cells circulates in the plasma; however, a proportion of VWF is anchored to the endothelial cell surface. Under conditions of physiological shear, endothelial-anchored VWF can bind to platelets, forming a VWF-platelet string that may represent the nidus of thrombus formation. A flow chamber system can be used to visually observe the release of VWF from endothelial cells and the subsequent platelet capture in a manner that is reproducible and relevant to the pathophysiology of VWF-mediated thrombus formation. Using this methodology, endothelial cells are cultured in a flow chamber and are subsequently stimulated with secretagogues to induce WPB exocytosis. Washed platelets are then perfused over the activated endothelium. The platelets are activated and subsequently bind to elongated VWF strings in the direction of fluid flow. Using extracellular histones as a procoagulant and proinflammatory stimulus, we observed increased VWF-platelet string formation on histone-treated endothelial cells compared to untreated endothelial cells. This protocol describes a quantitative, visual, and real-time assessment of the activation of VWF-platelet interactions in models of thrombosis and hemostasis.
MeSH term(s)	Blood Platelets/cytology ; Blood Platelets/metabolism ; Cell Culture Techniques/instrumentation ; Cell Culture Techniques/methods ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Endothelium, Vascular/cytology ; Enzyme-Linked Immunosorbent Assay/methods ; Exocytosis/physiology ; Hemostasis/physiology ; Histones/blood ; Histones/metabolism ; Humans ; Platelet Adhesiveness/physiology ; Thrombosis ; Weibel-Palade Bodies/metabolism ; von Willebrand Factor/metabolism
Chemical Substances	Histones ; von Willebrand Factor
Language	English
Publishing date	2017-08-14
Publishing country	United States
Document type	Journal Article ; Video-Audio Media
ISSN	1940-087X
ISSN (online)	1940-087X
DOI	10.3791/55917
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Article ; Online: The scavenger receptor SCARA5 is an endocytic receptor for von Willebrand factor expressed by littoral cells in the human spleen.

Swystun, Laura L / Ogiwara, Kenichi / Lai, Jesse D / Ojala, Juha R M / Rawley, Orla / Lassalle, Fanny / Notley, Colleen / Rengby, Olle / Michels, Alison / Nesbitt, Kate / Tryggvason, Karl / Lillicrap, David

Journal of thrombosis and haemostasis : JTH

2019 Volume 17, Issue 8, Page(s) 1384–1396

Abstract: Background: Scavenger receptors play a significant role in clearing aged proteins from the plasma, including the large glycoprotein coagulation factors von Willebrand factor (VWF) and factor VIII (FVIII). A large genome-wide association study meta- ... ...

Abstract	Background: Scavenger receptors play a significant role in clearing aged proteins from the plasma, including the large glycoprotein coagulation factors von Willebrand factor (VWF) and factor VIII (FVIII). A large genome-wide association study meta-analysis has identified genetic variants in the gene SCARA5, which encodes the class A scavenger receptor SCARA5, as being associated with plasma levels of VWF and FVIII. Objectives: The ability of SCARA5 to regulate the clearance of VWF-FVIII was characterized. Methods: VWF-FVIII interactions with SCARA5 were evaluated by solid phase binding assays and in vitro cell based assays. The influence of SCARA5 deficiency on VWF:Ag and half-life was assessed in a murine model. The expression pattern of SCARA5 and its colocalization with VWF was evaluated in human tissues. Results: VWF and the VWF-FVIII complex bound to human recombinant SCARA5 in a dose- and calcium-dependent manner. SCARA5 expressing HEK 293T cells bound and internalized VWF and the VWF-FVIII complex into early endosomes. In vivo, SCARA5 deficiency had a modest influence on the half-life of human VWF. mRNA analysis and immunohistochemistry determined that human SCARA5 is expressed in kidney podocytes and the red pulp, white pulp, and marginal zone of the spleen. VWF was found to colocalize with SCARA5 expressed by littoral cells lining the red pulp of the human spleen. Conclusions: SCARA5 is an adhesive and endocytic receptor for VWF. In human tissues, SCARA5 is expressed by kidney podocytes and splenic littoral endothelial cells. SCARA5 may have a modest influence on VWF clearance in humans.
MeSH term(s)	Animals ; Endocytosis ; Factor VIII/metabolism ; Female ; HEK293 Cells ; Humans ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Podocytes/metabolism ; Protein Binding ; Scavenger Receptors, Class A/genetics ; Scavenger Receptors, Class A/metabolism ; Spleen/cytology ; Spleen/metabolism ; von Willebrand Factor/metabolism
Chemical Substances	SCARA5 protein, human ; SCARA5 protein, mouse ; Scavenger Receptors, Class A ; von Willebrand Factor ; F8 protein, human (839MOZ74GK) ; Factor VIII (9001-27-8)
Language	English
Publishing date	2019-06-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1111/jth.14521
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Article ; Online: Reflections as near-peer facilitators of an inquiry project for undergraduate anatomy: Successes and challenges from a term of trial-and-error.

Anstey, Lauren M / Michels, Alison / Szymus, Julianna / Law, Wyanne / Edwin Ho, Man-Hymn / Qu, Fei / Yeung, Ralph T T / Chow, Natalie

Anatomical sciences education

2014 Volume 7, Issue 1, Page(s) 64–70

Abstract: Near-peer facilitators (senior students serving as facilitators to their more junior peers) bring a unique student-based perspective to teaching. With fewer years of teaching experience however, students who become involved in a facilitator role ... ...

Abstract	Near-peer facilitators (senior students serving as facilitators to their more junior peers) bring a unique student-based perspective to teaching. With fewer years of teaching experience however, students who become involved in a facilitator role typically develop related skills quickly through a process of trial-and-error within the classroom. The aim of this paper is to report on the authors' own experiences and reflections as student near-peer facilitators for an inquiry-based project in an undergraduate anatomy course. Three areas of the facilitator experience are explored: (1) offering adequate guidance as facilitators of inquiry, (2) motivating students to engage in the inquiry process, and (3) fostering creativity in learning. A practical framework for providing guidance to students is discussed which offers facilitators a scaffold for asking questions and assisting students through the inquiry process. Considerations for stimulating intrinsic motivations toward inquiry learning are made, paying attention to ways in which facilitators might influence feelings of motivation towards learning. Also, the role of creativity in inquiry learning is explored by highlighting the actions facilitators can take to foster a creative learning environment. Finally, recommendations are made for the development of formalized training programs that aid near-peer facilitators in the acquisition of facilitation skills before entering into a process of trial-and-error within the classroom.
MeSH term(s)	Anatomy/education ; Curriculum ; Humans ; Learning ; Motivation ; Peer Group ; Program Evaluation ; Students/psychology ; Teaching/methods
Language	English
Publishing date	2014-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2483491-9
ISSN	1935-9780 ; 1935-9772
ISSN (online)	1935-9780
ISSN	1935-9772
DOI	10.1002/ase.1383
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