ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Monocyte ADAM17 promotes diapedesis during transendothelial migration: identification of steps and substrates targeted by metalloproteinases.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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
21 citing papers in PubMed, 30 citations in OpenAlex.
- Leukocytic ADAM10 and ADAM17 modulate disease severity and systemic outcome in bacterial and viral pneumonia.The European respiratory journal · 2026Article
- Temporary effects of random positioning on the function and plasticity of proliferating monocytes.Scientific reports · 2025Article
- The function of metalloproteinases in pathophysiology of inflammatory bowel disease and colon cancer.Journal of leukocyte biology · 2025Review
- Survey of In Vitro Model Systems for Investigation of Key Cellular Processes Associated with Atherosclerosis.Methods in molecular biology (Clifton, N.J.) · 2022Article
- ADAM17 Boosts Cholesterol Efflux and Downstream Effects of High-Density Lipoprotein on Inflammatory Pathways in Macrophages.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Contribution of ADAM17 and related ADAMs in cardiovascular diseases.Cellular and molecular life sciences : CMLS · 2021Review
- ADAM10-Mediated Cleavage of ICAM-1 Is Involved in Neutrophil Transendothelial Migration.Cells · 2021Article
- Transcriptional Changes in CD16+ Monocytes May Contribute to the Pathogenesis of COVID-19.Frontiers in immunology · 2021Article
- An Allosteric Shift in CD11c Affinity Activates a Proatherogenic State in Arrested Intermediate Monocytes.Journal of immunology (Baltimore, Md. : 1950) · 2020Observational
- Neutrophil and Macrophage Cell Surface Colony-Stimulating Factor 1 Shed by ADAM17 Drives Mouse Macrophage Proliferation in Acute and Chronic Inflammation.Molecular and cellular biology · 2018Article
- Regulation of Leukocytes by TspanC8 Tetraspanins and the "Molecular Scissor" ADAM10.Frontiers in immunology · 2018Review
- ADAM10-Interacting Tetraspanins Tspan5 and Tspan17 Regulate VE-Cadherin Expression and Promote T Lymphocyte Transmigration.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Dopamine Increases CD14Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017Article
- Fine Tuning Cell Migration by a Disintegrin and Metalloproteinases.Mediators of inflammation · 2017Review
- Monocyte trafficking across the vessel wall.Cardiovascular research · 2015Review
- L-selectin shedding is activated specifically within transmigrating pseudopods of monocytes to regulate cell polarity in vitro.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
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- Real-time imaging of Toxoplasma-infected human monocytes under fluidic shear stress reveals rapid translocation of intracellular parasites across endothelial barriers.Cellular microbiology · 2014Article
- Ectoenzymes in leukocyte migration and their therapeutic potential.Seminars in immunopathology · 2014Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Despite expanded definition of the leukocyte adhesion cascade and mechanisms underlying individual steps, very little is known about regulatory mechanisms controlling sequential shifts between steps. We tested the hypothesis that metalloproteinases provide a mechanism to rapidly transition monocytes between different steps. Our study identifies diapedesis as a step targeted by metalloproteinase activity. Time-lapse video microscopy shows that the presence of a metalloproteinase inhibitor results in a doubling of the time required for human monocytes to complete diapedesis on unactivated or inflamed human endothelium, under both static and physiological-flow conditions. Thus, diapedesis is promoted by metalloproteinase activity. In contrast, neither adhesion of monocytes nor their locomotion over the endothelium is altered by metalloproteinase inhibition. We further demonstrate that metalloproteinase inhibition significantly elevates monocyte cell surface levels of integrins CD11b/CD18 (Mac-1), specifically during transendothelial migration. Interestingly, such alterations are not detected for other endothelial- and monocyte-adhesion molecules that are presumed metalloproteinase substrates. Two major transmembrane metalloproteinases, a disintegrin and metalloproteinase (ADAM)17 and ADAM10, are identified as enzymes that control constitutive cleavage of Mac-1. We further establish that knockdown of monocyte ADAM17, but not endothelial ADAM10 or ADAM17 or monocyte ADAM10, reproduces the diapedesis delay observed with metalloproteinase inhibition. Therefore, we conclude that monocyte ADAM17 facilitates the completion of transendothelial migration by accelerating the rate of diapedesis. We propose that the progression of diapedesis may be regulated by spatial and temporal cleavage of Mac-1, which is triggered upon interaction with endothelium.
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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.