Selectin on activated platelets enhances neutrophil endothelial adherence in myocardial reperfusion injury

• Published in: Cardiovascular research 1999-09, Vol.43 (4), p.968-973
• Main Authors: KOGAKI, S, SAWA, Y, SANO, T, MATSUSHITA, T, OHATA, T, KUROTOBI, S, TOJO, S. J, MATSUDA, H, OKADA, S
• Format: Article
• Language: English
• Subjects: Animals; Antibodies, Monoclonal - pharmacology; Biological and medical sciences; Blood Platelets - physiology; Cardiology. Vascular system; Cell Adhesion; Cell Movement; Cells, Cultured; Coculture Techniques; Coronary heart disease; Endothelium, Vascular - physiology; Heart; Male; Medical sciences; Mice; Myocardial Reperfusion Injury - pathology; Myocardial Reperfusion Injury - physiopathology; Myocardium - pathology; Neutrophils - physiology; P-Selectin - immunology; P-Selectin - physiology; Platelet Activation; Rats; Rats, Sprague-Dawley
• ISSN: 0008-6363; 1755-3245
• DOI: 10.1016/s0008-6363(99)00140-6

The glycoprotein P-selectin is an adhesion molecule that is rapidly expressed on the surface of platelets and endothelium during the inflammatory process. P-selectin on endothelium has been reported to play an important role in reperfusion injury. However, little is known regarding P-selectin on platelets in contributing to the pathophysiology of myocardial reperfusion injury. In this study, we hypothesized that P-selectin on platelets may enhance neutrophil endothelial adherence and this may play a role in neutrophil-mediated reperfusion injury. Endothelial cells, cardiomyocytes, platelets and neutrophils were isolated from adult rats. Endothelial cells and cardiomyocytes were cultivated in a co-culture system. After exposure to hypoxia and reoxygenation, neutrophil adherence and migration were examined. After exposure to 6 h of hypoxia, endothelial cells co-incubated with platelets showed significantly greater neutrophil adherence (63.1 +/- 4.0%) and migration (78.2 +/- 6.7%) than endothelial cells alone (adhesion: 44.2 +/- 2.8%, migration: 57.9 +/- 4.9%). These increases were significantly inhibited (adhesion: 42.1 +/- 3.5%, migration: 65.5 +/- 3.8%) by an anti-P-selectin monoclonal antibody. Moreover, the superoxide-anion production was significantly elevated when activated platelets were added to neutrophils. This enhanced production was also inhibited by anti-P-selectin antibody. The presence of activated platelets enhanced neutrophil adhesion and migration process after hypoxia reoxygenation. This process may occur following platelet-neutrophil interactions via P-selectin and subsequent neutrophil activation.