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Copyright © 2008 European Association for the Study of the Liver Published by Elsevier Ireland Ltd.
Additionally we present data about the behaviour of EC from different vascular beds and show EC morphology and behaviour under the fibrin clot.
![]() | PAI FEBS Letters |
![]() FEBS Letters, Volume 581, Issue 16, 26 June 2007, Pages 3098-3104 Hongtao Wang, Yan Zhang, Robert O. Heuckeroth Abstract Plasminogen activator inhibitor-1 (PAI-1) increases injury in several liver, lung and kidney disease models. The objective of this investigation was to assess the effect of PAI-1 deficiency on cholestatic liver fibrosis and determine PAI-1 influenced fibrogenic mechanisms. We found that PAI-1−/− mice had less fibrosis than wild type (WT) mice after bile duct ligation. This change correlated with increased tissue-type plasminogen activator (tPA) activity, and increased matrix metalloproteinase-9 (MMP-9), but not MMP-2 activity. Furthermore, there was increased activation of the tPA substrate hepatocyte growth factor (HGF), a known anti-fibrogenic protein. In contrast, there was no difference in hepatic urokinase plasminogen activator (uPA) or plasmin activities between PAI-1−/− and WT mice. There was also no difference in the level of transforming growth factor beta 1 (TGF-β1), stellate cell activation or collagen production between WT and PAI-1−/− animals. In conclusion, PAI-1 deficiency reduces hepatic fibrosis after bile duct obstruction mainly through the activation of tPA and HGF. ![]() |
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