Identification of Domains Responsible for von Willebrand Factor Type VI Collagen Interaction Mediating Platelet Adhesion under High Flow

Mazzucato, M.; Spessotto, Paola; Masotti, Adriana; Appollonia, Leandro De; Cozzi, Marzia; Yoshioka, Akira; Perris, Roberto; Colombatti, Alfonso; Marco, Luigi De

doi:10.1074/jbc.274.5.3033

Cited by 77 publications

(78 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Collagen type VI serves as substrate for the attachment of cells and for anchoring collagen fibers, nerve and blood vessels to the surrounding connective tissue [13,14]. In vascular tissues, collagen type VI is a primary subendothelial extracellular matrix component, responsible for von Willebrand factor (vWF)-dependent platelet adhesion and aggregation under high tensile strength [18,24,25,34]. Dysregulation of collagen VI synthesis can be an important contributing factor in the complex mechanisms of disordered matrix protein deposition leading to tissue fibrosis [l 1, 27,28,30,35,36], and thus has at least a candidate role in the pathogenesis of the SSCT changes seen in patients with CTS.…”

Section: Discussionmentioning

confidence: 99%

Immunolocalization of collagen types in the subsynovial connective tissue within the carpal tunnel in humans

Jinrok¹,

Zhao²,

Amadio³

et al. 2005

Journal Orthopaedic Research

View full text Add to dashboard Cite

The tenosynovium within the carpal tunnel consists of a single layer of synovial cells, which lines the bursae within the carpal tunnel, and the subsynovial connective tissue (SSCT), which contains the tendon vasculature and other structural elements. In this study, we used immunogold labeling to localize collagen types within the SSCT in three cadaver specimens and three patients with carpal tunnel syndrome. Positive labeling for collagen types I, 111 and VI was found with immunoelectron microscopy. Collagen types I and 111 were codistributed within the SSCT. Type VI was primarily located in microfibrillar structures between collagen bundles, between elastin and collagen bundles and between collagen bundles and cells. There was no difference in the distribution of collagen types when comparing cadaver specimens and carpal tunnel patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Immunolocalization of collagen types in the subsynovial connective tissue within the carpal tunnel in humans

Jinrok¹,

Zhao²,

Amadio³

et al. 2005

Journal Orthopaedic Research

View full text Add to dashboard Cite

show abstract

“…Native laminin-1-nidogen complex from Engelbreth-Holm-Swarm mouse tumor was obtained as previously described (36). Chick COLL VI tetramers were purified as previously described (37). Tenascin and human perlecan were kindly provided by Luciano Zardi (Advanced Biotechnology Centre, Genoa, Italy) and Anders Malmström (Lund University Hospital, Lund, Sweden), respectively.…”

Section: Abs and Reagentsmentioning

confidence: 99%

An Alternative Role of C1q in Cell Migration and Tissue Remodeling: Contribution to Trophoblast Invasion and Placental Development

Agostinis

Bulla²,

Tripodo

et al. 2010

The Journal of Immunology

Self Cite

140

132

View full text Add to dashboard Cite

“…First, in an ex vivo study using blood from VWF-deficient pigs, a defect in platelet deposition at low shear rate (200 to 400 s Ϫ1 ) was demonstrated, 26 and second, in a flow chamber coated with collagen type VI, platelet adhesion was shown to be VWF dependent at a shear rate of 100 s Ϫ1 . 27 In order to form a thrombus, the important parameter is not the number of transiently tethering platelets to the injured vessel wall but the number of platelets that are stably adherent because of ␣IIb␤3 activation. Previously, it was shown in vitro that on type I collagen fibrils thrombus growth at low shear is dependent on integrin ␣IIb␤3 and GPIb␣ and that VWF was less relevant.…”

Section: Role Of Vwf In Venous Thrombosis 2427mentioning

confidence: 99%

von Willebrand factor and factor VIII are independently required to form stable occlusive thrombi in injured veins

Chauhan

Kisucka

Lamb

et al. 2006

Blood

View full text Add to dashboard Cite

von Willebrand factor (VWF) protects factor VIII (FVIII) from proteolysis and mediates the initial contact of platelets with the injured vessel wall, thus playing an important role in hemostasis and thrombosis. VWF is crucial for the formation of occlusive thrombi at arterial shear rates. However, with only a few conflicting studies published, the role of VWF in venous thrombosis is still unclear. Using genetargeted mice, we show that in ferric chloride-injured veins platelet adhesion to subendothelium is decreased and thrombus growth is impaired in VWF ؊/؊ mice when compared with wild type (WT). We also observed increased embolization in the VWF ؊/؊ mice, which was due to lower FVIII levels in these mice as recombinant factor VIII (r-FVIII) restored thrombus stability. Despite normalization of blood clotting time and thrombus stability after r-FVIII infusion, the VWF ؊/؊ venules did not occlude. Introductionvon Willebrand factor (VWF) is a large adhesive glycoprotein synthesized in megakaryocytes and endothelial cells and stored in platelet ␣-granules and Weibel-Palade bodies, respectively. VWF circulates in plasma as a series of multimers ranging from 500 to 20 000 kDa. The size of the multimers is regulated through proteolysis 1,2 by a specific protease ADAMTS13 (a disintegrin-like and metalloprotease with thrombospondin type I repeats-13). [3][4][5] There are 3 pools of VWF: (1) soluble plasma VWF, (2) subendothelial (ECM) VWF, and (3) cellular VWF in storage granules. 6 VWF is a carrier for factor VIII (FVIII) and protects it from inactivation. 7 The formation of a thrombus on an injured vessel wall is a complex process that involves multiple adhesion molecules (VWF, collagen, fibrinogen, and fibronectin) and their respective receptors on the platelet surface (GPIb␣, GPVI, ␤1 and ␤3 integrins). VWF has 2 main receptors, GPIb␣ in the GPIb-IX-V complex and the integrin ␣IIb␤3. 8 Pathological thrombosis can occur in arteries and veins. Arterial thrombosis is often linked to inappropriate platelet activation and can result in myocardial infarction and ischemic stroke, while venous thrombosis (eg, deep vein thrombosis) is commonly linked to high procoagulant activity, which produces fibrin-rich thrombi. In the clinical setting, elevated levels of FVIII and VWF are associated with an increased risk of venous thrombosis. The Leiden Thrombophilia Study suggested that the effect of elevated VWF on the risk of venous thrombosis was due to increased FVIII levels. 9 In contrast, the Longitudinal Investigation of Thromboembolism Etiology (LITE) Study showed FVIII and VWF were independently associated with venous thromboembolism. 10 Under high shear, the VWF-GPIb␣ interaction is necessary for initial platelet contact with the subendothelium, while irreversible platelet aggregation also requires interaction between the VWF and integrin ␣IIb␤3. 8,[11][12][13] Although an important role for VWF in platelet-platelet cohesion and thrombus formation at arterial shear rates was demonstrated both in vitro 13,14 and in vivo, 15,...

show abstract

Identification of Domains Responsible for von Willebrand Factor Type VI Collagen Interaction Mediating Platelet Adhesion under High Flow

Cited by 77 publications

References 66 publications

Immunolocalization of collagen types in the subsynovial connective tissue within the carpal tunnel in humans

Immunolocalization of collagen types in the subsynovial connective tissue within the carpal tunnel in humans

An Alternative Role of C1q in Cell Migration and Tissue Remodeling: Contribution to Trophoblast Invasion and Placental Development

von Willebrand factor and factor VIII are independently required to form stable occlusive thrombi in injured veins

Contact Info

Product

Resources

About