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Plasminogen activation in venous leg ulcers.
Y Herouy1, D Trefzer, M O Hellstern
1Department of Dermatology, University of Freiburg, Hauptstr. 7, 79104 Freiburg, Germany. herouy@haut.ukl.uni-freiburg.de
The British Journal of Dermatology
|November 9, 2000
Summary
Venous leg ulcers show increased urokinase-type plasminogen activator (uPA) and its receptor (uPAR). This suggests plasminogen activation is key to the ulcer
Area of Science:
- Wound healing research
- Biochemistry of tissue repair
- Vascular biology
Background:
- Venous leg ulcers stem from chronic venous insufficiency.
- Matrix metalloproteinase-2 (MMP-2) is implicated in ulcer pathogenesis.
- MMP-2 activation involves urokinase-type plasminogen activator (uPA) and its receptor (uPAR).
Purpose of the Study:
- To investigate the role of plasminogen activation in venous leg ulcers.
- To clarify the expression and activity of key plasminogen activators in ulcer tissue.
Main Methods:
- Analysis of uPA, uPAR, tPA, PAI-1, and PAI-2 expression via RT-PCR and Western blotting.
- Immunohistochemical detection of uPA and uPAR.
- Assessment of endogenous uPA activity using fibrin zymography.
Main Results:
- Elevated mRNA and protein levels of uPA and uPAR in venous leg ulcers compared to healthy skin.
- Increased immunohistochemical staining for uPA and uPAR in ulcer tissue.
- Significantly higher endogenous uPA activity observed in venous leg ulcers.
Conclusions:
- Venous leg ulcers exhibit heightened plasminogen activation.
- This enzyme cascade is crucial for maintaining proteolytic activity in these ulcers.
- Findings suggest targeting plasminogen activation could be a therapeutic strategy.