Submitted on February 8, 2007
Accepted on May 8, 2007
Exercise Modulates Platelet-Nasopharyngeal Carcinoma Cell Aggregation and Subsequent Tissue Factor and Matrix Metalloproteinase Activities
Jong Shyan Wang1*, Chuen Ying Chang2, Shu Er Chow3, Yu-Wen Chen4, and Chuen-Mao Yang5
1 Graduate Institute of Rehabilitation Science and Center for Gerontological Research, Chang Gung University, Tao-Yuan, Taiwan, Taiwan - Republic of China
2 Graduate Institute of Rehabilitation Science and Center for Gerontological Research, Chang Gung University, Tao-Yuan, Taiwan - Republic of China
3 Department of Physiology, Chang Gung University, Tao-Yuan, Taiwan - Republic of China
4 Graduate Institute of Rehabilitation Science, Chang Gung University, Taiwan - Republic of China
5 Pharmacology, Chang Gung University, Tao-Yuan, United States; Pharmacology, Chang Gung University, 259 Wen-Hwa 1st Road, Kwei-San, Tao-Yuan, 3332
* To whom correspondence should be addressed. E-mail: s5492{at}mail.cgu.edu.tw.
Interaction between platelet and carcinoma cell contributes to pathogenesis of cancer-related thrombosis and metastasis. This study investigated whether physical exercise affects platelet-nasopharyngeal carcinoma cell (NPC) interaction and platelet-promoted tissue factor (TF) and matrix metalloproteinase (MMP) activities of NPC. Thirty sedentary men performed on three occasions moderate-intensity exercise (MIE, 60% VO2max for 40 min) and high-intensity exercise (HIE, up to VO2max) with and without warm-up exercise (WUE, 60% VO2max for 20 min) on a bicycle ergometer. Before and immediately after exercise, platelet-NPC aggregation, the TF, MMP-2, and MMP-9 expressions and activities, and tissue factor pathway inhibitor (TFPI) and tissue inhibitor of MMP-1 (TIMP-1) levels of NPC and platelet were measured. The results of this study demonstrated that HIE enhanced platelet-NPC aggregation in the presence of fibrinogen, was accompanied by increased platelet-promoted TF activity and expression of NPC and decreased platelet-promoted MMP-2 and MMP-9 activities and TFPI release of NPC, whereas these alterations to HIE on platelet-NPC interactions were ameliorated by WUE pretreatment. Conversely, MIE reduced the formation of platelet-NPC aggregates, but did not change the TF, TFPI, MMP-2 and MMP-9, and TIMP-1 activities and/or levels of NPC mediated by platelet. It is concluded that HIE may enhance aggregation and coagulation, and reduce MMP bioactivity related with platelet-NPC interactions, by raising the binding affinity to fibrinogen and TF activity and expression, and lowering TFPI release and MMP-2 and -9 activities. These effects on HIE diminish after WUE. However, MIE minimizes the risk of thrombosis induced by platelet-NPC interactions.
