ArticleJournal of thrombosis and haemostasis : JTH2011
Interaction of fibrin with VE-cadherin and anti-inflammatory effect of fibrin-derived fragments.
Article in Journal of thrombosis and haemostasis : JTH, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- FX06 to rescue SARS-CoV-2-induced acute respiratory distress syndrome: a randomized clinical trial.Critical care (London, England) · 2023Trial
- Vascular leakage during circulatory failure: physiopathology, impact and treatments.Annals of intensive care · 2025Review
- Identification of Neural (N)-Cadherin as a Novel Endothelial Cell Receptor for Fibrin and Localization of the Complementary Binding Sites.Biochemistry · 2024Article
- Platelet factor 4 improves survival in a murine model of antibiotic-susceptible and methicillin-resistantFrontiers in cellular and infection microbiology · 2023Article
- Current View on the Molecular Mechanisms Underlying Fibrin(ogen)-Dependent Inflammation.Thrombosis and haemostasis · 2022Review
- Fibrinogen and Factor XIII in Venous Thrombosis and Thrombus Stability.Arteriosclerosis, thrombosis, and vascular biology · 2022Review
- Dual functions of the fibrin βN-domains in the VLDL receptor-dependent pathway of transendothelial migration of leukocytes.Thrombosis research · 2022Article
- Relation of αInternational journal of molecular sciences · 2020Article
- Resuscitative Strategies to Modulate the Endotheliopathy of Trauma: From Cell to Patient.Shock (Augusta, Ga.) · 2020Review
- Fibrin-VLDL Receptor-Dependent Pathway Promotes Leukocyte Transmigration by Inhibiting Src Kinase Fyn and is a Target for Fibrin β15-42 Peptide.Thrombosis and haemostasis · 2019Article
- Fibrin Nanoparticles Coupled with Keratinocyte Growth Factor Enhance the Dermal Wound-Healing Rate.ACS applied materials & interfaces · 2019Article
- Effect of fibrinogen, fibrin, and fibrin degradation products on transendothelial migration of leukocytes.Thrombosis research · 2018Article
- Genetically Engineered Phage Induced Selective H9c2 Cardiomyocytes Patterning in PDMS Microgrooves.Materials (Basel, Switzerland) · 2017Article
- Article
- Fibrin Formation, Structure and Properties.Sub-cellular biochemistry · 2017Review
- Anti-VLDL receptor monoclonal antibodies inhibit fibrin-VLDL receptor interaction and reduce fibrin-dependent leukocyte transmigration.Thrombosis and haemostasis · 2016Article
- Fibrinogen Is at the Interface of Host Defense and Pathogen Virulence in Staphylococcus aureus Infection.Seminars in thrombosis and hemostasis · 2016Review
- Interaction of Fibrin with the Very Low Density Lipoprotein Receptor: Further Characterization and Localization of the Fibrin-Binding Site.Biochemistry · 2015Article
- Article
- Structure and function of fibrinogen BβN-domains.Ukrainian biochemical journalArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe interaction of the fibrin βN-domain with VE-cadherin on endothelial cells is implicated in transendothelial migration of leukocytes, and the β15-42 fragment representing part of this domain has been shown to inhibit this process. However, our previous study revealed that only a dimeric (β15-66)(2) fragment, corresponding to the full-length βN-domain and mimicking its dimeric arrangement in fibrin, bound to VE-cadherin.
objectiveTo test our hypothesis that dimerization of β15-42-containing fragments increases their affinity for VE-cadherin and ability to inhibit transendothelial migration of leukocytes.
methodsInteraction of β15-42-containing fragments with VE-cadherin was characterized by ELISA and surface plasmon resonance. The inhibitory effect of such fragments was tested in vitro with a leukocyte transendothelial migration assay and in vivo with mouse models of peritonitis and myocardial ischemia-reperfusion injury.
resultsFirst, we prepared the monomeric β15-42 and β15-64 fragments and their dimeric forms, (β15-44)(2) and (β15-66)(2) , and studied their interaction with the fibrin-binding domain of VE-cadherin, VE-cad(3). The experiments revealed that both dimeric fragments bound to VE-cad(3) with high affinity, whereas the affinities of β15-42 and β15-64 were significantly lower. Next, we tested the ability of these fragments to inhibit leukocyte transmigration in vitro and infiltration into the inflamed peritoneum in vivo, and found that the inhibitory effects of the dimers on these processes were also superior. Furthermore, (β15-44)(2) significantly reduced myocardial injury induced by ischemia-reperfusion.
conclusionThe results confirm our hypotheses and indicate that (β15-66)(2) and (β15-44)(2) , which exhibited much higher affinity for VE-cadherin, are highly effective in suppressing inflammation by inhibiting leukocyte transmigration.
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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.