Homophilic Interaction Between Transmembrane-JAM-A and Soluble JAM-A Regulates Thrombo-Inflammation: Implications for Coronary Artery Disease

Genetic predisposition through F11R-single-nucleotide variation (SNV) influences circulatory soluble junctional adhesion molecule-A (sJAM-A) levels in coronary artery disease (CAD) patients. Homozygous carriers of the minor alleles (F11R-SNVs rs2774276, rs790056) show enhanced levels of thrombo-infl...

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Detalles Bibliográficos
Autores principales: Rath, Dominik, Rapp, Vera, Schwartz, Jessica, Winter, Stefan, Emschermann, Frederic, Arnold, Daniel, Rheinlaender, Johannes, Büttcher, Manuela, Strebl, Michael, Braun, Michael B., Altgelt, Konstanze, Uribe, Álvaro Petersen, Schories, Christoph, Canjuga, Denis, Schaeffeler, Elke, Borst, Oliver, Schäffer, Tilman E., Langer, Harald, Stehle, Thilo, Schwab, Matthias, Geisler, Tobias, Gawaz, Meinrad, Chatterjee, Madhumita
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2022
Materias:
Leading Edge Translational Research
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9156439/
https://www.ncbi.nlm.nih.gov/pubmed/35663628
http://dx.doi.org/10.1016/j.jacbts.2022.03.003
Descripción
Sumario:Genetic predisposition through F11R-single-nucleotide variation (SNV) influences circulatory soluble junctional adhesion molecule-A (sJAM-A) levels in coronary artery disease (CAD) patients. Homozygous carriers of the minor alleles (F11R-SNVs rs2774276, rs790056) show enhanced levels of thrombo-inflammatory sJAM-A. Both F11R-SNVs and sJAM-A are associated with worse prognosis for recurrent myocardial infarction in CAD patients. Platelet surface-associated JAM-A correlate with platelet activation markers in CAD patients. Activated platelets shed transmembrane-JAM-A, generating proinflammatory sJAM-A and JAM-A-bearing microparticles. Platelet transmembrane-JAM-A and sJAM-A as homophilic interaction partners exaggerate thrombotic and thrombo-inflammatory platelet monocyte interactions. Therapeutic strategies interfering with this homophilic interface may regulate thrombotic and thrombo-inflammatory platelet response in cardiovascular pathologies where circulatory sJAM-A levels are elevated.

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