ArticleBiophysical journal2016
Glycoprotein Ib-IX-V Complex Transmits Cytoskeletal Forces That Enhance Platelet Adhesion.
Article in Biophysical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 65 citations in OpenAlex.
- Mechanotransduction of Magnetically Applied Forces Leads to Mechanical Stiffening of Platelet-Rich Plugs.Advanced healthcare materials · 2026Article
- Utility of point-of-care platelet aggregation testing for transfusion prediction.Scientific reports · 2026Article
- F-actin disassembly by the oxidoreductase MICAL1 promotes mechano-dependent VWF-GPIbα interaction in platelets.Nature communications · 2025Article
- Von Willebrand Factor Collagen-Binding Activity and Von Willebrand Factor-Mediated Platelet Adhesion in Patients with Coronary Artery Disease.Biomedicines · 2024Article
- Contractility defects hinder glycoprotein VI-mediated platelet activation and affect platelet functions beyond clot contraction.Research and practice in thrombosis and haemostasis · 2024Article
- Is glycoprotein VI involved in contractual negotiations?Research and practice in thrombosis and haemostasis · 2024Article
- Using microfluidic shear to assess transfusion requirements in trauma patients.Trauma surgery & acute care open · 2024Article
- Detection of cellular traction forces via the force-triggered Cas12a-mediated catalytic cleavage of a fluorogenic reporter strand.Nature biomedical engineering · 2023Article
- Molecular mechanisms of catch bonds and their implications for platelet hemostasis.Biophysical reviews · 2023Review
- Distinct platelet F-actin patterns and traction forces on von Willebrand factor versus fibrinogen.Biophysical journal · 2023Article
- Why platelet mechanotransduction matters for hemostasis and thrombosis.Journal of thrombosis and haemostasis : JTH · 2023Review
- An Updated Review on Glycoprotein IIb/IIIa Inhibitors as Antiplatelet Agents: Basic and Clinical Perspectives.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2023Review
- Structure, signal transduction, activation, and inhibition of integrin αIIbβ3.Thrombosis journal · 2023Review
- Nanofiber Topographies Enhance Platelet-Fibrinogen Scaffold Interactions.Advanced healthcare materials · 2022Article
- Reduced platelet forces underlie impaired hemostasis in mouse models ofScience advances · 2022Article
- Variations in the Gene Expression Profile in Atherosclerotic Patients with Non-Fatal ACS: A Preliminary Study.International journal of molecular sciences · 2022Article
- A guide to molecular and functional investigations of platelets to bridge basic and clinical sciences.Nature cardiovascular research · 2022Article
- Ex vivo anticoagulants affect human blood platelet biomechanics with implications for high-throughput functional mechanophenotyping.Communications biology · 2022Article
- Filamin A in platelets: Bridging the (signaling) gap between the plasma membrane and the actin cytoskeleton.Frontiers in molecular biosciences · 2022Review
- Platelet Dysfunction During Mechanical Circulatory Support: Elevated Shear Stress Promotes Downregulation of αArteriosclerosis, thrombosis, and vascular biology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Platelets bind to exposed vascular matrix at a wound site through a highly specialized surface receptor, glycoprotein (GP) Ib-IX-V complex, which recognizes von Willebrand factor (VWF) in the matrix. GPIb-IX-V is a catch bond for it becomes more stable as force is applied to it. After attaching to the wound site, platelets generate cytoskeletal forces to compact and reinforce the hemostatic plug. Here, we evaluated the role of the GPIb-IX-V complex in the transmission of cytoskeletal forces. We used arrays of flexible, silicone nanoposts to measure the contractility of individual platelets on VWF. We found that a significant proportion of cytoskeletal forces were transmitted to VWF through GPIb-IX-V, an unexpected finding given the widely held notion that platelet forces are transmitted exclusively through its integrins. In particular, we found that the interaction between GPIbα and the A1 domain of VWF mediates this force transmission. We also demonstrate that the binding interaction between GPIbα and filamin A is involved in force transmission. Furthermore, our studies suggest that cytoskeletal forces acting through GPIbα are involved in maintaining platelet adhesion when external forces are absent. Thus, the GPIb-IX-V/VWF bond is able to transmit force, and uses this force to strengthen the bond through a catch-bond mechanism. This finding expands our understanding of how platelets attach to sites of vascular injury, describing a new, to the best of our knowledge, mechanism in which the catch bonds of GPIb-IX-V/VWF can be supported by internal forces produced by cytoskeletal tension.
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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.