Human platelets release TGFBIp in acute myocardial infarction

• Published in: Heart and vessels Vol. 37; no. 11; pp. 1962 - 1970
• Main Authors: Kraemer, Bjoern F., Martinovic, Ivo, Lindemann, Stephan
• Format: Journal Article
• Language: English
• Published: Tokyo Springer Japan 01.11.2022; Springer Nature B.V
• Subjects: Acute coronary syndromes; Arteries; Biomedical Engineering and Bioengineering; Blood platelets; Cardiac Surgery; Cardiology; Collagen; Complications; Embolism; Enzyme-linked immunosorbent assay; Flow chambers; Growth factors; Heart attacks; Immunoblotting; Medicine; Medicine & Public Health; Myocardial infarction; Original Article; Platelets; Proteins; Vascular Surgery; Platelets; Acute coronary syndrome; Transforming growth factor; Migration
• ISSN: 0910-8327; 1615-2573
• DOI: 10.1007/s00380-022-02086-z

Transforming growth factor-β-induced protein (TGFBIp) is released from activated platelets and promotes pro-thrombotic complications like pulmonary embolism. The role of TGFBIp in acute coronary syndrome, especially with a focus on platelets, has not been investigated so far. Using ELISA and immunoblotting, we demonstrate platelet TGFBIp release in patients with myocardial infarction (MI). We investigated TGFBIp-induced platelet adhesion and rolling by flow chamber and chemotactic effects of TGFBIp in transwell experiments. Immunochemistry staining of arterial vessels detected TGFBIp and the platelet-specific protein GPVI in the vessel wall.We demonstrate for the first time that platelet TGFBIp release is significantly increased in MI and correlates with the severity of acute coronary syndromes (STEMI, NSTEMI). After activation with TRAP, platelets release TGFBIp and TGFBIp itself activates platelets. Under flow, TGFBIp-mediated platelet rolling and adherence similarly to collagen. TGFBIp significantly increased platelet transmigration and we demonstrate TGFBIp deposits in the wall of human arteries. In this study, we add novel aspects to the role of TGFBIp in acute coronary syndrome by demonstrating that TGFBIp is partially released from platelets during MI and has activating, pro-adhesive and pro-migratory effects on platelets that could contribute to the disease development of coronary vascular inflammation and MI.