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

Autor:	Rath D; Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany., Rapp V; Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany., Schwartz J; Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany., Winter S; Dr Margarete Fischer-Bosch Institute of Clinical Pharmacology, Stuttgart, and University of Tübingen, Tübingen, Germany., Emschermann F; Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany., Arnold D; Institute of Applied Physics, University of Tübingen, Tübingen, Germany., Rheinlaender J; Institute of Applied Physics, University of Tübingen, Tübingen, Germany., Büttcher M; Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany., Strebl M; Interfaculty Institute of Biochemistry, University of Tübingen, Tübingen, Germany., Braun MB; Interfaculty Institute of Biochemistry, University of Tübingen, Tübingen, Germany., Altgelt K; Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany., Uribe ÁP; Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany., Schories C; Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany., Canjuga D; Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany., Schaeffeler E; Dr Margarete Fischer-Bosch Institute of Clinical Pharmacology, Stuttgart, and University of Tübingen, Tübingen, Germany., Borst O; Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany.; DFG Heisenberg Group Thrombocardiology, Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany., Schäffer TE; Institute of Applied Physics, University of Tübingen, Tübingen, Germany., Langer H; Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany., Stehle T; Interfaculty Institute of Biochemistry, University of Tübingen, Tübingen, Germany., Schwab M; Dr Margarete Fischer-Bosch Institute of Clinical Pharmacology, Stuttgart, and University of Tübingen, Tübingen, Germany.; Department of Pharmacy and Biochemistry, University of Tübingen, Tübingen, Germany.; Department of Clinical Pharmacology, University Hospital Tübingen, Tübingen, Germany., Geisler T; Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany., Gawaz M; Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany., Chatterjee M; Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany.
Jazyk:	angličtina
Zdroj:	JACC. Basic to translational science [JACC Basic Transl Sci] 2022 May 23; Vol. 7 (5), pp. 445-461. Date of Electronic Publication: 2022 May 23 (Print Publication: 2022).
DOI:	10.1016/j.jacbts.2022.03.003
Abstrakt:	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. Competing Interests: The project was supported by funding from Deutsche Stiftung für Herzforschung (DSHF-F/22/17) to Dr Chatterjee; Deutsche Gesellschaft für Kardiologie-DGK-Otto Hess Promotionstipendium to Dr Rapp; Robert Bosch Stiftung to Drs Winter, Schaeffeler, and Schwab; and Deutsche Forschungsgemeinschaft-190538538, SCHW858/1-2, BO3786/3-1, and DFG-374031971–TRR-240. All other authors have reported that they have no relationships relevant to the contents of this paper. (© 2022 The Authors.)
Databáze:	MEDLINE
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