ArticleArteriosclerosis, thrombosis, and vascular biology2013
Neuroimmune guidance cue Semaphorin 3E is expressed in atherosclerotic plaques and regulates macrophage retention.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.
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Who cites it
77 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.
- Systems Genetics Analysis of Genome-Wide Association Study Reveals Novel Associations Between Key Biological Processes and Coronary Artery Disease.Arteriosclerosis, thrombosis, and vascular biology · 2015Pooled it
- Serum semaphorin 7A is associated with the risk of acute atherothrombotic stroke.Journal of cellular and molecular medicine · 2019Trial
- Integrated multi-omics identifies lineage-dependent myeloid cells recruitment and the APP-CD74 axis as an immunoregulatory target in pediatric high-grade glioma.Acta neuropathologica · 2026Article
- Immunometabolism in obesity: Understanding the beneficial and detrimental roles of inflammation.PLoS biology · 2026Article
- How lactate and lactylation shape the immunity system in atherosclerosis (Review).International journal of molecular medicine · 2025Review
- Mechanisms and consequences of myeloid adhesome dysfunction in atherogenesis.Cardiovascular research · 2025Article
- Neuroimmune circuits in the plaque and bone marrow regulate atherosclerosis.Cardiovascular research · 2025Review
- Inflammation in atherosclerosis: a Big Idea that has underperformed so far.Current opinion in lipidology · 2025Review
- Targeting Unc5b in macrophages drives atherosclerosis regression and pro-resolving immune cell function.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- [Beyond the plaque: immunological implications of risk factors in atherosclerosis].Archivos de cardiologia de Mexico · 2024Review
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Programmed death of macrophages in atherosclerosis: mechanisms and therapeutic targets.Nature reviews. Cardiology · 2024Review
- Phytol from3 Biotech · 2024Article
- Inflammation Resolution in the Cardiovascular System: Arterial Hypertension, Atherosclerosis, and Ischemic Heart Disease.Antioxidants & redox signaling · 2024Review
- Review
- A Lipid-Structured Model of Atherosclerotic Plaque Macrophages with Lipid-Dependent Kinetics.Bulletin of mathematical biology · 2023Article
- Plexin D1 mediates disturbed flow-induced M1 macrophage polarization in atherosclerosis.Heliyon · 2023Article
- The diverse roles of macrophages in metabolic inflammation and its resolution.Frontiers in cell and developmental biology · 2023Review
- Semaphorins in immune cell function, inflammatory and infectious diseases.Current research in immunology · 2023Review
- RGMa promotes dedifferentiation of vascular smooth muscle cells into a macrophage-like phenotype in vivo and in vitro.Journal of lipid research · 2022Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe persistence of myeloid-derived cells in the artery wall is a characteristic of advanced atherosclerotic plaques. However, the mechanisms by which these cells are retained are poorly understood. Semaphorins, a class of neuronal guidance molecules, play a critical role in vascular patterning and development, and recent studies suggest that they may also have immunomodulatory functions. The present study evaluates the expression of Semaphorin 3E (Sema3E) in settings relevant to atherosclerosis and its contribution to macrophage accumulation in plaques. APPROACH AND
resultsImmunofluorescence staining of Sema3E, and its receptor PlexinD1, demonstrated their expression in macrophages of advanced atherosclerotic lesions of Apoe(-/-) mice. Notably, in 2 different mouse models of atherosclerosis regression, Sema3E mRNA was highly downregulated in plaque macrophages, coincident with a reduction in plaque macrophage content and an enrichment in markers of reparative M2 macrophages. In vitro, Sema3E mRNA was highly expressed in inflammatory M1 macrophages and in macrophages treated with physiological drivers of plaque progression and inflammation, such as oxidized low-density lipoprotein and hypoxia. To explore mechanistically how Sema3E affects macrophage behavior, we treated macrophages with recombinant protein in the presence/absence of chemokines, including CCL19, a chemokine implicated in the egress of macrophages from atherosclerotic plaques. Sema3E blocked actin polymerization and macrophage migration stimulated by the chemokines, suggesting that it may immobilize these cells in the plaque.
conclusionsSema3E is upregulated in macrophages of advanced plaques, is dynamically regulated by multiple atherosclerosis-relevant factors, and acts as a negative regulator of macrophage migration, which may promote macrophage retention and chronic inflammation in vivo.
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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.