Thromb Haemost 1997; 78(02): 934-938
DOI: 10.1055/s-0038-1657655
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Perturbation of Platelet Adhesion to Endothelial Cells by Plasminogen Activation In Vitro

Hsiun-ing Chen
1  The Department of Physiology, National Cheng-Kung University, Tainan, Taiwan, ROC
,
Yueh-I Wu
1  The Department of Physiology, National Cheng-Kung University, Tainan, Taiwan, ROC
,
Yu-Lun Hsieh
1  The Department of Physiology, National Cheng-Kung University, Tainan, Taiwan, ROC
,
Guey-Yueh Shi
2  The Department of Biochemistry, National Cheng-Kung University, Tainan, Taiwan, ROC
,
Meei-Jyh Jiang
3  The Department of Anatomy, National Cheng-Kung University, Tainan, Taiwan, ROC
,
Wen-Chang Chang
4  The Department of Pharmacology, National Cheng-Kung University, Tainan, Taiwan, ROC
,
Woei-Jer Chuang
2  The Department of Biochemistry, National Cheng-Kung University, Tainan, Taiwan, ROC
,
Wai-Ming Kan
4  The Department of Pharmacology, National Cheng-Kung University, Tainan, Taiwan, ROC
,
Ming-Jer Tang
1  The Department of Physiology, National Cheng-Kung University, Tainan, Taiwan, ROC
,
Chauying J Jen
1  The Department of Physiology, National Cheng-Kung University, Tainan, Taiwan, ROC
› Author Affiliations
Further Information

Publication History

Received 07 1997

Accepted after revision 17 March 1997

Publication Date:
12 July 2018 (online)

Summary

To investigate whether the endothelium-platelet interactions may be altered by plasminogen activation, cultured human umbilical vein endothelial cells (ECs) were treated with tissue-type plasminogen activator (t-PA) in the presence of plasminogen, and platelet adhesion to ECs was subsequently measured by using a tapered flow chamber. Our results demonstrated that platelets adhered more readily to t-PA treated EC monolayer than to the control monolayer at all shear stress levels tested. This phenomenon was treatment time-dependent and dose-dependent, and it could be blocked by adding plasmin inhibitors, such as e-amino caproic acid and aprotinin. Adherent platelets on t-PA treated EC monolayer underwent more severe shape change than those on the control monolayer. While the extracellular matrix directly treated with t-PA attracted less platelets than the control matrix did, platelet adhesion to the matrix that was produced by t-PA-treated ECs was unaltered. These data suggest that t-PA treatment on ECs compromised antiplatelet-adhesion capability on their apical surface without altering the reactivity of their extracellular matrix towards platelets.