Tissue plasminogen activator induced by dengue virus infection of human endothelial cells

2003 ◽  
Vol 70 (4) ◽  
pp. 610-616 ◽  
Author(s):  
Ying-Huey Huang ◽  
Huan-Yao Lei ◽  
Hsiao-Sheng Liu ◽  
Yee-Shin Lin ◽  
Shun-Hua Chen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Virus Infection ◽  
Dengue Virus ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Human Endothelial Cells ◽  
Dengue Virus Infection ◽  
Tissue Plasminogen

Specificity of the Thrombin-Induced Release of Tissue Plasminogen Activator from Cultured Human Endothelial Cells

1986 ◽  
Vol 56 (02) ◽  
pp. 115-119 ◽  
Author(s):  
Eugene G Levin ◽  
David M Stern ◽  
Peter P Nawroth ◽  
Richard A Marlar ◽  
Daryl S Fair ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Protein C ◽  
Primary Cultures ◽  
Activated Protein C ◽  
Specific Inhibitor ◽  
Factor Xa ◽  
Human Endothelial Cells ◽  
Tissue Plasminogen

SummaryThe addition of thrombin (9 nM) to primary cultures of human endothelial cells induces a 6- to 7-fold increase in the rate of release of tissue plasminogen activator (tPA). Several other serine proteases which specifically interact with endothelial cells were also analyzed for their effect on tPA release. Gamma-thrombin, an autocatalytic product of α-thrombin, promoted tPA release but was less effective than α-thrombin. A maximum increase of 5.5-fold was observed, although a concentration of γ-thrombin 20 times greater than α-thrombin was required. The response to Factor Xa was similar to α-thrombin, although the stimulation was significantly reduced by the addition of hirudin or DAPA suggesting that prothrombin activation was occurring. The simultaneous addition of prothrombin with Factor Xa resulted in enhanced tPA release equal to that observed with an equimolar concentration of active α-thrombin. Thus, under these conditions, Factor Xa-cell surface mediated activation of prothrombin can lead to a secondary effect resulting from cell-thrombin interaction. Activated protein C, which has been implicated as a profibrinolytic agent, was also tested. No change in tPA release occurred after the addition of up to 325 nM activated protein C in the presence or absence of proteins. Factor IXa and plasmin were also ineffective. The effect of thrombin on the endothelial cell derived plasminogen activator specific inhibitor was also studied. Thrombin produced a small but variable release of the inhibitor with an increase of less than twice that of non-thrombin treated controls.

scholarly journals The Ubiquitin−Proteasome Pathway Is Important for Dengue Virus Infection in Primary Human Endothelial Cells

2010 ◽  
Vol 9 (10) ◽  
pp. 4960-4971 ◽  
Author(s):  
Rattiyaporn Kanlaya ◽  
Sa-nga Pattanakitsakul ◽  
Supachok Sinchaikul ◽  
Shui-Tein Chen ◽  
Visith Thongboonkerd
Keyword(s):  
Endothelial Cells ◽  
Virus Infection ◽  
Dengue Virus ◽  
Human Endothelial Cells ◽  
Dengue Virus Infection ◽  
Ubiquitin Proteasome Pathway ◽  
Ubiquitin Proteasome ◽  
Proteasome Pathway
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