Evaluation of gingival crevicular fluid levels of tissue plasminogen activator, plasminogen activator inhibitor 2, matrix metalloproteinase-3 and interleukin 1-β in patients with different periodontal diseases

2014 ◽  
Vol 50 (1) ◽  
pp. 44-51 ◽  
Author(s):  
U. Toyman ◽  
G. Tüter ◽  
B. Kurtiş ◽  
E. Kıvrak ◽  
Ş. Bozkurt ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Gingival Crevicular Fluid ◽  
Periodontal Diseases ◽  
Interleukin 1 ◽  
Plasminogen Activator Inhibitor ◽  
Matrix Metalloproteinase 3 ◽  
Tissue Plasminogen ◽  
Crevicular Fluid ◽  
Fluid Levels ◽  
Activator Inhibitor

Herpes Simplex Virus Decreases Endothelial Cell Plasminogen Activator Inhibitor

1993 ◽  
Vol 69 (03) ◽  
pp. 253-258 ◽  
Author(s):  
Robert A Bok ◽  
Harry S Jacob ◽  
Jozsef Balla ◽  
Margaret Juckett ◽  
Theresa Stelle ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Umbilical Vein ◽  
Plasminogen Activator Inhibitor ◽  
Tissue Plasminogen ◽  
Simplex Virus ◽  
Activator Inhibitor ◽  
Pai 1

SummaryHerpes simplex virus (HSV) infection is histopathologically associated with vascular injury, fibrinoid necrosis and inflammatory cell infiltrates. We have previously shown in vitro that HSV infection of human umbilical vein endothelial cells (HUVEC) promotes a procoagulant phenotype manifest by the induction of tissue factor, the loss of thrombomodulin, and an increase in platelet adhesion. In these studies we examined the effects of HSV infection on HUVEC plasminogen activator inhibitor type 1 (PAI-1) and tissue plasminogen activator (t-PA). HSV infection caused the loss of PAI-1 in the extracellular matrix (ECM) and that released into the supernatant of HUVEC. Both activity and antigen levels of the Serpin inhibitor are diminished as a result of HSV infection. The loss of inhibitor is not secondary to diminished vitronectin (Vn), the primary binding protein of PAI-1 in the ECM, but appears to be secondary to decreased synthesis at the RNA level. Tissue plasminogen activator (t-PA). synthesis is also decreased in endothelial HSV infection. PAI-1 loss may further promote a procoagulant phenotype in HSV infection in vivo.

Localization of Fibrinolytic Activators and Inhibitors in Normal and Atherosclerotic Vessels

1996 ◽  
Vol 75 (06) ◽  
pp. 933-938 ◽  
Author(s):  
Marten Fålkenberg ◽  
Johan Tjärnstrom ◽  
Per Örtenwall ◽  
Michael Olausson ◽  
Bo Risberg
Keyword(s):  
Endothelial Cells ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Vasa Vasorum ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Tissue Plasminogen ◽  
The Media ◽  
Activator Inhibitor ◽  
Pai 1

SummaryLocal fibrinolytic changes in atherosclerotic arteries have been suggested to influence plaque growth and promote mural thrombosis on ruptured or ulcerated plaques. Increased levels of plasminogen activator inhibitor (PAI-1) have been found in atherosclerotic arteries. In this study tissue plasminogen activator (t-PA), urokinase-type plasminogen activator (u-PA) and PAI-1 were localized in arterial biopsies of healthy and atherosclerotic vessels by immunohistochemis-try. The expression of fibrinolytic regulators was related to the distribution of endothelial cells (EC) and macrophages. Results: t-PA was expressed in vasa vasorum. PAI-1 was positive in endothelial cells, in the media and in the adventitia. Increased expression of t-PA, u-PA and PAI-1 was found in atherosclerotic vessels. t-PA, u-PA, PAI-1 and macrophages were co-localized in plaques. These results support the concept that macrophages can be important in the local regulation of fibrinolysis in atherosclerotic vessels.

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