ArticleArteriosclerosis, thrombosis, and vascular biology2015
Fibrin, γ'-fibrinogen, and transclot pressure gradient control hemostatic clot growth during human blood flow over a collagen/tissue factor wound.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- A three-dimensional shear dependent continuum model of platelet aggregation under flow.PLoS computational biology · 2026Article
- High fibrinogen γ' levels in patient plasma increase clot formation at arterial and venous shear.Blood advances · 2021Article
- Core and shell platelets of a thrombus: A new microfluidic assay to study mechanics and biochemistry.Research and practice in thrombosis and haemostasis · 2020Article
- Src family kinases inhibition by dasatinib blocks initial and subsequent platelet deposition on collagen under flow, but lacks efficacy with thrombin generation.Thrombosis research · 2020Article
- A Mathematical Model of Bivalent Binding Suggests Physical Trapping of Thrombin within Fibrin Fibers.Biophysical journal · 2019Article
- Microfluidic and computational study of structural properties and resistance to flow of blood clots under arterial shear.Biomechanics and modeling in mechanobiology · 2019Article
- Reduced model to predict thrombin and fibrin during thrombosis on collagen/tissue factor under venous flow: Roles of γ'-fibrin and factor XIa.PLoS computational biology · 2019Article
- Establishing the Transient Mass Balance of Thrombosis: From Tissue Factor to Thrombin to Fibrin Under Venous Flow.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Impact of Tissue Factor Localization on Blood Clot Structure and Resistance under Venous Shear.Biophysical journal · 2018Article
- Contact Pathway Function During Human Whole Blood Clotting on Procoagulant Surfaces.Frontiers in medicine · 2018Review
- Probing the Dynamics of Clot-Bound Thrombin at Venous Shear Rates.Biophysical journal · 2017Article
- Fibrinogen and Fibrin in Hemostasis and Thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2017Review
- Article
- Fibrin Formation, Structure and Properties.Sub-cellular biochemistry · 2017Review
- Dynamics of Thrombin Generation and Flux from Clots during Whole Human Blood Flow over Collagen/Tissue Factor Surfaces.The Journal of biological chemistry · 2016Article
- Transport physics and biorheology in the setting of hemostasis and thrombosis.Journal of thrombosis and haemostasis : JTH · 2016Review
- Primed to Understand Fibrinogen in Cardiovascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveBiological and physical factors interact to modulate blood response in a wounded vessel, resulting in a hemostatic clot or an occlusive thrombus. Flow and pressure differential (ΔP) across the wound from the lumen to the extravascular compartment may impact hemostasis and the observed core/shell architecture. We examined physical and biological factors responsible for regulating thrombin-mediated clot growth. APPROACH AND
resultsUsing factor XIIa-inhibited human whole blood perfused in a microfluidic device over collagen/tissue factor at controlled wall shear rate and ΔP, we found thrombin to be highly localized in the P-selectin(+) core of hemostatic clots. Increasing ΔP from 9 to 29 mm Hg (wall shear rate=400 s(-1)) reduced P-selectin(+) core size and total clot size because of enhanced extravasation of thrombin. Blockade of fibrin polymerization with 5 mmol/L Gly-Pro-Arg-Pro dysregulated hemostasis by enhancing both P-selectin(+) core size and clot size at 400 s(-1) (20 mm Hg). For whole-blood flow (no Gly-Pro-Arg-Pro), the thickness of the P-selectin-negative shell was reduced under arterial conditions (2000 s(-1), 20 mm Hg). Consistent with the antithrombin-1 activity of fibrin implicated with Gly-Pro-Arg-Pro, anti-γ'-fibrinogen antibody enhanced core-localized thrombin, core size, and overall clot size, especially at venous (100 s(-1)) but not arterial wall shear rates (2000 s(-1)). Pathological shear (15 000 s(-1)) and Gly-Pro-Arg-Pro synergized to exacerbate clot growth.
conclusionsHemostatic clotting was dependent on core-localized thrombin that (1) triggered platelet P-selectin display and (2) was highly regulated by fibrin and the transclot ΔP. Also, γ'-fibrinogen had a role in venous but not arterial conditions.
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