{Reference Type}: Journal Article
{Title}: Homophilic Interaction Between Transmembrane-JAM-A and Soluble JAM-A Regulates Thrombo-Inflammation: Implications for Coronary Artery Disease.
{Author}: Rath D;Rapp V;Schwartz J;Winter S;Emschermann F;Arnold D;Rheinlaender J;Büttcher M;Strebl M;Braun MB;Altgelt K;Uribe ÁP;Schories C;Canjuga D;Schaeffeler E;Borst O;Schäffer TE;Langer H;Stehle T;Schwab M;Geisler T;Gawaz M;Chatterjee M;
{Journal}: JACC Basic Transl Sci
{Volume}: 7
{Issue}: 5
{Year}: May 2022
{Factor}: 9.531
{DOI}: 10.1016/j.jacbts.2022.03.003
{Abstract}: 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.