ArticlePloS one2018
MASP-1 of the complement system enhances clot formation in a microvascular whole blood flow model.
Article in PloS one, 2018. 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.
- Is COVID-19 Coagulopathy a Thrombotic Microangiopathy? A Prospective, Observational Study.International journal of molecular sciences · 2025Observational
- MASP1 modulation as a novel therapeutic target in severe pediatric pertussis: insights from a multi-omics approach.Infection and immunity · 2025Article
- Vascular dysfunction in hemorrhagic viral fevers: opportunities for organotypic modeling.Biofabrication · 2024Review
- The Lectin Pathway of the Complement System-Activation, Regulation, Disease Connections and Interplay with Other (Proteolytic) Systems.International journal of molecular sciences · 2024Review
- Plasma levels of mannan-binding lectin-associated serine proteases are increased in type 1 diabetes patients with insulin resistance.Clinical and experimental immunology · 2024Article
- Unveiling the Great Therapeutic Potential of MASPs as Hemostatic Agents.Journal of hematology · 2022Article
- Targeting thromboinflammation in COVID-19 - A narrative review of the potential of C1 inhibitor to prevent disease progression.Molecular immunology · 2022Review
- Distinction of early complement classical and lectin pathway activationFrontiers in immunology · 2022Article
- Complement lectin pathway components MBL and MASP-1 promote haemostasis upon vessel injury in a microvascular bleeding model.Frontiers in immunology · 2022Article
- Thromboinflammation Model-on-A-Chip by Whole Blood Microfluidics on Fixed Human Endothelium.Diagnostics (Basel, Switzerland) · 2021Article
- Renal diseases and the role of complement: Linking complement to immune effector pathways and therapeutics.Advances in immunology · 2021Review
- MASPs at the crossroad between the complement and the coagulation cascades - the case for COVID-19.Genetics and molecular biology · 2021Article
- Does Complement-Mediated Hemostatic Disturbance Occur in Traumatic Brain Injury? A Literature Review and Observational Study Protocol.International journal of molecular sciences · 2020Review
- Exploring the structural similarity yet functional distinction between coagulation factor XIII-B and complement factor H sushi domains.Journal of thrombosis and thrombolysis · 2019Article
- Novel MASP-2 inhibitors developed via directed evolution of human TFPI1 are potent lectin pathway inhibitors.The Journal of biological chemistry · 2019Article
- Article
- Mannose-Binding Lectin Drives Platelet Inflammatory Phenotype and Vascular Damage After Cerebral Ischemia in Mice via IL (Interleukin)-1α.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Be on Target: Strategies of Targeting Alternative and Lectin Pathway Components in Complement-Mediated Diseases.Frontiers in immunology · 2018Review
- The Lectin Pathway of Complement in Myocardial Ischemia/Reperfusion Injury-Review of Its Significance and the Potential Impact of Therapeutic Interference by C1 Esterase Inhibitor.Frontiers in immunology · 2018Review
- Diabetes affects endothelial cell function and alters fibrin clot formation in a microvascular flow model: A pilot study.Diabetes & vascular disease researchArticle
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement and coagulation systems closely interact with each other. These interactions are believed to contribute to the proinflammatory and prothrombotic environment involved in the development of thrombotic complications in many diseases. Complement MASP-1 (mannan-binding lectin-associated serine protease-1) activates coagulation factors and promotes clot formation. However, this was mainly shown in purified or plasma-based static systems. Here we describe the role of MASP-1 and complement activation in fibrin clot formation in a microvascular, whole blood flow model. This microfluidic system simulates blood flow through microvessels at physiological flow and shear rates and represents the closest model system to human physiology so far. It features parallel microchannels cultured with endothelial cells in a transparent microfluidic chip allowing real-time evaluation of clot formation by confocal microscopy. To test their effects on clot formation, we added the following activators or inhibitors (individually or in combination) to whole blood and performed perfusion experiments: rMASP-1cf (recombinant active form of MASP-1), complement activator zymosan, selective MASP-1 inhibitor SGMI-1 (based on the Schistocerca gregaria protease inhibitor scaffold), classical pathway inhibitor rSALO (recombinant salivary anti-complement from Lutzomyia longipalpis). Addition of rMASP-1cf resulted in accelerated fibrin clot formation while addition of SGMI-1 delayed it. Complement activation by zymosan led to increased clot formation and this effect was partially reversed by addition of rSALO and almost abolished in combination with SGMI-1. We show for the first time a strong influence of MASP-1, complement activation and pathway-specific inhibition on coagulation in a microvascular flow system that is closest to human physiology, further underpinning the in vivo relevance of coagulation and complement interactions.
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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.