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Purpose of Review <p>Cell-cell adhesion between leukocytes, platelets and endothelial cells plays a critical role in vascular inflammation and thrombus formation. This review aims at providing a comprehensive picture of the contribution of the immunoglobulin superfamily (IgSF) cell adhesion receptor Junctional Adhesion Molecule-A (JAM-A) to the process of atherosclerosis.</p> Recent Findings <p>Proinflammatory and proatherogenic stimulation of endothelial cells results in redistribution of JAM-A from cell-cell junctions to the apical surface to promote monocyte adhesion and transmigration. Agonist-stimulation of platelets results in elevated surface levels of JAM-A concomitant with enhanced release of soluble JAM-A (sJAM-A). sJAM-A promotes platelet aggregation, thrombus formation, and platelet-monocyte aggregate formation. Elevated levels of sJAM-A correlate with recurrent myocardial infarction.</p> Summary <p>JAM-A is expressed by several cell types implicated in atherogenesis, notably endothelial cells, platelets, and leukocytes. Proinflammatory and proatherogenic stimuli induce a redistribution of JAM-A within endothelial cells. Stimulated platelets release sJAM-A into the circulation. This review illustrates the role of JAM-A in atherogenesis and elaborates the underlying mechanisms.</p>

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JAM-A: Adhesion Receptor and Signaling Regulator in Atherosclerosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月29日

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  • Mariel F. Schwietzer,
  • Klaus Ebnet

摘要

Purpose of Review

Cell-cell adhesion between leukocytes, platelets and endothelial cells plays a critical role in vascular inflammation and thrombus formation. This review aims at providing a comprehensive picture of the contribution of the immunoglobulin superfamily (IgSF) cell adhesion receptor Junctional Adhesion Molecule-A (JAM-A) to the process of atherosclerosis.

Recent Findings

Proinflammatory and proatherogenic stimulation of endothelial cells results in redistribution of JAM-A from cell-cell junctions to the apical surface to promote monocyte adhesion and transmigration. Agonist-stimulation of platelets results in elevated surface levels of JAM-A concomitant with enhanced release of soluble JAM-A (sJAM-A). sJAM-A promotes platelet aggregation, thrombus formation, and platelet-monocyte aggregate formation. Elevated levels of sJAM-A correlate with recurrent myocardial infarction.

Summary

JAM-A is expressed by several cell types implicated in atherogenesis, notably endothelial cells, platelets, and leukocytes. Proinflammatory and proatherogenic stimuli induce a redistribution of JAM-A within endothelial cells. Stimulated platelets release sJAM-A into the circulation. This review illustrates the role of JAM-A in atherogenesis and elaborates the underlying mechanisms.