%0 Journal Article
%T Homophilic Interaction Between Transmembrane-JAM-A and Soluble JAM-A Regulates Thrombo-Inflammation: Implications for Coronary Artery Disease.
%A Rath D
%A Rapp V
%A Schwartz J
%A Winter S
%A Emschermann F
%A Arnold D
%A Rheinlaender J
%A Büttcher M
%A Strebl M
%A Braun MB
%A Altgelt K
%A Uribe ÁP
%A Schories C
%A Canjuga D
%A Schaeffeler E
%A Borst O
%A Schäffer TE
%A Langer H
%A Stehle T
%A Schwab M
%A Geisler T
%A Gawaz M
%A Chatterjee M
%J JACC Basic Transl Sci
%V 7
%N 5
%D May 2022
%M 35663628
%F 9.531
%R 10.1016/j.jacbts.2022.03.003
%X 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.