Homophilic Interaction Between Transmembrane-JAM-A and Soluble JAM-A Regulates Thrombo-Inflammation: Implications for Coronary Artery Disease.
JACC Basic Transl Sci
; 7(5): 445-461, 2022 May.
Article
em En
| MEDLINE
| ID: mdl-35663628
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.
ACM, all-cause mortality; ACS, acute coronary syndrome; ADP, adenosine diphosphate; CAD, coronary artery disease; CCS, chronic coronary syndrome; CE, combined endpoint; HC, homozygous carriers; IS, ischemic stroke; JAM-A; JAM-A, junctional adhesion molecule-A; MI, myocardial infarction; SNV; SNV, single-nucleotide variation; TRAP, thrombin receptor activating peptide; coronary artery disease; platelet; sJAM-A, soluble junctional adhesion molecule-A; smJAM-A, soluble murine junctional adhesion molecule-A; thrombo-inflammation
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1
Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Revista:
JACC Basic Transl Sci
Ano de publicação:
2022
Tipo de documento:
Article
País de afiliação:
Alemanha