ArticleThe American journal of pathology2015
Human mannose-binding lectin inhibitor prevents myocardial injury and arterial thrombogenesis in a novel animal model.
Article in The American journal of pathology, 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, 31 citations in OpenAlex.
- Antibodies to mannose-binding lectin and factor XI Inhibit Shiga toxin-induced kidney injury additively in a murine model.Pediatric research · 2026Article
- The Lectin Pathway of the Complement System-Activation, Regulation, Disease Connections and Interplay with Other (Proteolytic) Systems.International journal of molecular sciences · 2024Review
- Complement inhibition can decrease the haemostatic response in a microvascular bleeding model at multiple levels.Frontiers in immunology · 2023Article
- Targeting thromboinflammation in COVID-19 - A narrative review of the potential of C1 inhibitor to prevent disease progression.Molecular immunology · 2022Review
- Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting complement activation and upregulation of miR-499.Experimental and therapeutic medicine · 2021Article
- A Plausible Role for Collectins in Skin Immune Homeostasis.Frontiers in immunology · 2021Review
- Mannose-Binding Lectin is Associated with Thrombosis and Coagulopathy in Critically Ill COVID-19 Patients.Thrombosis and haemostasis · 2020Article
- Novel MASP-2 inhibitors developed via directed evolution of human TFPI1 are potent lectin pathway inhibitors.The Journal of biological chemistry · 2019Article
- The Human Platelet as an Innate Immune Cell: Interactions Between Activated Platelets and the Complement System.Frontiers in immunology · 2019Review
- Article
- 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
- Complement Dependence of Murine Costimulatory Blockade-Resistant Cellular Cardiac Allograft Rejection.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2017Article
- Activation of complement factor B contributes to murine and human myocardial ischemia/reperfusion injury.PloS one · 2017Article
- Ischemia/Reperfusion.Comprehensive Physiology · 2016Review
- Human mannose-binding lectin inhibitor prevents Shiga toxin-induced renal injury.Kidney international · 2016Article
- Strong predictive value of mannose-binding lectin levels for cardiovascular risk of hemodialysis patients.Journal of translational medicine · 2016Article
- Variant mapping and mutation discovery in inbred mice using next-generation sequencing.BMC genomics · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Myocardial infarction and coagulation disorders are leading causes of disability and death in the world. An important role of the lectin complement pathway in myocardial infarction and coagulation has been demonstrated in mice genetically deficient in lectin complement pathway proteins. However, these studies are limited to comparisons between wild-type and deficient mice and lack the ability to examine reversal/inhibition of injury after disease establishment. We developed a novel mouse that expresses functional human mannose-binding lectin (MBL) 2 under the control of Mbl1 promoter. Serum MBL2 concentrations averaged approximately 3 μg/mL in MBL2(+/+)Mbl1(-/-)Mbl2(-/-) [MBL2 knock in (KI)] mice. Serum MBL2 level in MBL2 KI mice significantly increased after 7 (8 μg/mL) or 14 (9 μg/mL) days of hyperglycemia compared to normoglycemic mice (P < 0.001). Monoclonal antibody 3F8 inhibited C3 deposition on mannan-coated plates in MBL2 KI, but not wild-type, mice. Myocardial ischemia/reperfusion in MBL2 KI mice revealed that 3F8 preserved cardiac function and decreased infarct size and fibrin deposition in a time-dependent manner. Furthermore, 3F8 prevented ferric chloride-induced occlusive arterial thrombogenesis in vivo. MBL2 KI mice represent a novel animal model that can be used to study the lectin complement pathway in acute and chronic models of human disease. Furthermore, these novel mice demonstrate the therapeutic window for MBL2 inhibition for effective treatment of disease and its complications.
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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.