ArticlePloS one2016
Divergent JAM-C Expression Accelerates Monocyte-Derived Cell Exit from Atherosclerotic Plaques.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Flow-based imaging reveals dissociated monocyte adhesion and transmigration patterns between TNF-α and diabetes-induced vascular inflammation.Frontiers in immunology · 2026Article
- Type 2 Diabetes Mellitus Impairs the Reverse Transendothelial Migration Capacity (rTEM) of Inflammatory CD14Cells · 2025Article
- Junctional adhesion molecule-C: A multifunctional mediator of cell adhesion.Cellular and molecular life sciences : CMLS · 2025Review
- sJAM-C as a Potential Biomarker for Coronary Artery Stenosis: Insights from a Clinical Study in Coronary Heart Disease Patients.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Monocyte Differentiation and Heterogeneity: Inter-Subset and Interindividual Differences.International journal of molecular sciences · 2023Review
- The diverse roles of macrophages in metabolic inflammation and its resolution.Frontiers in cell and developmental biology · 2023Review
- Exploration of the shared gene signatures and molecular mechanisms between atherosclerosis and rheumatoid arthritis via multi-microarray data analyses.Annals of translational medicine · 2022Article
- Perspectives on Vascular Regulation of Mechanisms Controlling Selective Immune Cell Function in the Tumor Immune Response.International journal of molecular sciences · 2022Review
- Junctional Adhesion Molecules: Potential Proteins in Atherosclerosis.Frontiers in cardiovascular medicine · 2022Review
- The Roles of Junctional Adhesion Molecules (JAMs) in Cell Migration.Frontiers in cell and developmental biology · 2022Review
- Dynamic trafficking and turnover of JAM-C is essential for endothelial cell migration.PLoS biology · 2019Article
- Atherosclerosis: integration of its pathogenesis as a self-perpetuating propagating inflammation: a review.Cardiovascular endocrinology & metabolism · 2019Review
- Methods to Study Monocyte and Macrophage Trafficking in Atherosclerosis Progression and Resolution.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Macrophage Trafficking, Inflammatory Resolution, and Genomics in Atherosclerosis: JACC Macrophage in CVD Series (Part 2).Journal of the American College of Cardiology · 2018Review
- Angiogenic factor-driven inflammation promotes extravasation of human proangiogenic monocytes to tumours.Nature communications · 2018Article
- Macrophages in vascular inflammation and atherosclerosis.Pflugers Archiv : European journal of physiology · 2017Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Atherosclerosis, caused in part by monocytes in plaques, continues to be a disease that afflicts the modern world. Whilst significant steps have been made in treating this chronic inflammatory disease, questions remain on how to prevent monocyte and macrophage accumulation in atherosclerotic plaques. Junctional Adhesion Molecule C (JAM-C) expressed by vascular endothelium directs monocyte transendothelial migration in a unidirectional manner leading to increased inflammation. Here we show that interfering with JAM-C allows reverse-transendothelial migration of monocyte-derived cells, opening the way back out of the inflamed environment. To study the role of JAM-C in plaque regression we used a mouse model of atherosclerosis, and tested the impact of vascular JAM-C expression levels on monocyte reverse transendothelial migration using human cells. Studies in-vitro under inflammatory conditions revealed that overexpression or gene silencing of JAM-C in human endothelium exposed to flow resulted in higher rates of monocyte reverse-transendothelial migration, similar to antibody blockade. We then transplanted atherosclerotic, plaque-containing aortic arches from hyperlipidemic ApoE-/- mice into wild-type normolipidemic recipient mice. JAM-C blockade in the recipients induced greater emigration of monocyte-derived cells and further diminished the size of atherosclerotic plaques. Our findings have shown that JAM-C forms a one-way vascular barrier for leukocyte transendothelial migration only when present at homeostatic copy numbers. We have also shown that blocking JAM-C can reduce the number of atherogenic monocytes/macrophages in plaques by emigration, providing a novel therapeutic strategy for chronic inflammatory pathologies.
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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.