© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Selectin on activated platelets enhances neutrophil endothelial adherence in myocardial reperfusion injury
aDepartment of Pediatrics, Faculty of Medicine, Osaka University 2-2, Yamada-oka Suita, Osaka 565-0871, Japan
bThe First Department of Surgery, Faculty of Medicine, Osaka University, Osaka, Japan
cSumitomo Pharmaceuticals Research Center, Osaka, Japan
* Corresponding author. Tel.: +81-6-879-3936; fax: +81-6-879-3939
Objectives: 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. Methods: 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. Results: 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. Conclusion: 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.
KEYWORDS Experimental; Heart; Pathophysiology; Cell communication; Leukocytes; Platelets; Reperfusion; Rat
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