ArticleArteriosclerosis, thrombosis, and vascular biology2009
Junctional adhesion molecule-C mediates leukocyte infiltration in response to ischemia reperfusion injury.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 64 citations in OpenAlex.
- Junctional adhesion molecule-C: A multifunctional mediator of cell adhesion.Cellular and molecular life sciences : CMLS · 2025Review
- Unraveling the deadly dance: endothelial cells and neutrophils in sepsis-induced acute lung injury/acute respiratory distress syndrome.Frontiers in cell and developmental biology · 2025Review
- Effects of neutrophil fate on inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Targeting Neutrophils for Promoting the Resolution of Inflammation.Frontiers in immunology · 2022Review
- The Roles of Junctional Adhesion Molecules (JAMs) in Cell Migration.Frontiers in cell and developmental biology · 2022Review
- Soluble JAM-C Ectodomain Serves as the Niche for Adipose-Derived Stromal/Stem Cells.Biomedicines · 2021Article
- β2 Integrin Regulation of Neutrophil Functional Plasticity and Fate in the Resolution of Inflammation.Frontiers in immunology · 2021Review
- Neutrophil heterogeneity and fate in inflamed tissues: implications for the resolution of inflammation.American journal of physiology. Cell physiology · 2020Article
- Renal damage after liver transplantation.Bioscience reports · 2020Article
- Protein Palmitoylation in Leukocyte Signaling and Function.Frontiers in cell and developmental biology · 2020Review
- Dynamic trafficking and turnover of JAM-C is essential for endothelial cell migration.PLoS biology · 2019Article
- Targeting junctional adhesion molecule-C ameliorates sepsis-induced acute lung injury by decreasing CXCR4Journal of leukocyte biology · 2018Article
- Review
- Ischemia-reperfusion injury in stroke: impact of the brain barriers and brain immune privilege on neutrophil function.Therapeutic advances in neurological disorders · 2018Review
- Identification of novel molecular signatures of IgA nephropathy through an integrative -omics analysis.Scientific reports · 2017Article
- Endothelial Cell Junctional Adhesion Molecules: Role and Regulation of Expression in Inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2016Review
- Divergent JAM-C Expression Accelerates Monocyte-Derived Cell Exit from Atherosclerotic Plaques.PloS one · 2016Article
- Leukotriene B4-Neutrophil Elastase Axis Drives Neutrophil Reverse Transendothelial Cell Migration In Vivo.Immunity · 2015Article
- Acute kidney injury.Journal of injury & violence research · 2015Article
- Blocking junctional adhesion molecule C enhances dendritic cell migration and boosts the immune responses against Leishmania major.PLoS pathogens · 2014Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
objectiveJunctional adhesion molecule-C (JAM-C) is an adhesion molecule that has multiple roles in inflammation and vascular biology, but many aspects of its functions under pathological conditions are unknown. Here we investigated the role of JAM-C in leukocyte migration in response to ischemia reperfusion (I/R) injury. METHODS AND
resultsPretreatment of mice with soluble JAM-C (sJAM-C), used as a pharmacological blocker of JAM-C-mediated reactions, significantly suppressed leukocyte migration in models of kidney and cremaster muscle I/R injury (39 and 51% inhibition, respectively). Furthermore, in the cremaster muscle model (studied by intravital microscopy), both leukocyte adhesion and transmigration were suppressed in JAM-C-deficient mice (JAM-C(-/-)) and enhanced in mice overexpressing JAM-C in their endothelial cells (ECs). Analysis of JAM-C subcellular expression by immunoelectron microscopy indicated that in I/R-injured tissues, EC JAM-C was redistributed from cytoplasmic vesicles and EC junctional sites to nonjunctional plasma membranes, a response that may account for the role of JAM-C in both leukocyte adhesion and transmigration under conditions of I/R injury.
conclusionsThe findings demonstrate a role for EC JAM-C in mediating leukocyte adhesion and transmigration in response to I/R injury and indicate the existence of a novel regulatory mechanism for redistribution and hence function of EC JAM-C 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.