ArticleJournal of the American Heart Association2014
Antiphospholipid antibodies attenuate endothelial repair and promote neointima formation in mice.
Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Mechanism of antiphospholipid antibody-mediated thrombosis in antiphospholipid syndrome.Frontiers in immunology · 2025Review
- Interaction of antiphospholipid antibodies with endothelial cells in antiphospholipid syndrome.Frontiers in immunology · 2024Review
- Exploration of the Effect on Genome-Wide DNA Methylation byInternational journal of molecular sciences · 2021Article
- New Insights in the Pathophysiology of Antiphospholipid Syndrome.Seminars in thrombosis and hemostasis · 2018Review
- Article
- Cellular and Molecular Mechanisms of Anti-Phospholipid Syndrome.Frontiers in immunology · 2018Review
- Delayed reendothelialization with rapamycin is rescued by the addition of nicorandil in balloon-injured rat carotid arteries.Oncotarget · 2016Article
- Soluble analog of ApoER2 targeting beta2-glycoprotein I in immune complexes counteracts hypertension in lupus-prone mice with spontaneous antiphospholipid syndrome.Journal of thrombosis and haemostasis : JTH · 2016Article
- Loss of Reelin protects against atherosclerosis by reducing leukocyte-endothelial cell adhesion and lesion macrophage accumulation.Science signaling · 2016Article
- Identification of a Monoclonal Antibody That Attenuates Antiphospholipid Syndrome-Related Pregnancy Complications and Thrombosis.PloS one · 2016Article
- An A1-A1 mutant with improved binding and inhibition of β2GPI/antibody complexes in antiphospholipid syndrome.The FEBS journal · 2015Article
- Evaluation of anticardiolipin antibodies in tobacco users and non-tobacco users with severe chronic periodontal disease.Journal of International Society of Preventive & Community DentistryArticle
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundAntiphospholipid syndrome patients have antiphospholipid antibodies (aPLs) that promote thrombosis, and they have increased cardiovascular disease risk. Although the basis for the thrombosis has been well delineated, it is not known why antiphospholipid syndrome patients also have an increased prevalence of nonthrombotic vascular occlusion. The aims of this work were to determine if aPLs directly promote medial hypertrophy or neointima formation in mice and to identify the underlying mechanisms. METHODS AND
resultsMedial hypertrophy and neointima formation invoked by carotid artery endothelial denudation were evaluated in mice administered normal human IgG or aPLs. While aPLs had no effect on medial hypertrophy, they caused exaggerated neointima development. This was related to an aPL-induced impairment in reendothelialization post denudation, and scratch assays in cell culture revealed that there are direct effects of aPLs on endothelium that retard cell migration. Further experiments showed that aPL antagonism of endothelial migration and repair is mediated by antibody recognition of β2-glycoprotein I, apolipoprotein E receptor 2, and a decline in bioavailable NO. Consistent with these mechanisms, the adverse impacts of aPLs on reendothelialization and neointima formation were fully prevented by the NO donor molsidomine.
conclusionsAPLs blunt endothelial repair, and there is related aPL-induced exaggeration in neointima formation after endothelial injury in mice. The initiating process entails NO deficiency mediated by β2-glycoprotein I recognition by aPLs and apolipoprotein E receptor 2. The modulation of endothelial apolipoprotein E receptor 2 function or NO bioavailability may represent new interventions to prevent the nonthrombotic vascular occlusion and resulting cardiovascular disorders that afflict antiphospholipid syndrome patients.
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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.