Histone deacetylase inhibitors stimulate tissue-type plasminogen activator production in vascular endothelial cells

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• 作者：Pia Larsson (1)
  Niklas Bergh (1)
  Emma Lu (1)
  Erik Ulfhammer (1)
  Mia Magnusson (1)
  Karin W?hlander (2)
  Lena Karlsson (1)
  Sverker Jern (1) (3)
  
• 关键词：Fibrinolysis ; Tissue ; type plasminogen activator ; Endothelial cell ; HDAC inhibitor
• 刊名：Journal of Thrombosis and Thrombolysis
• 出版年：2013
• 出版时间：February 2013
• 年：2013
• 卷：35
• 期：2
• 页码：185-192
• 全文大小：538KB
• 参考文献：1. WHO (2011) World Health Organization Fact sheet 310: The top 10 causes of death
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• 作者单位：Pia Larsson (1)
  Niklas Bergh (1)
  Emma Lu (1)
  Erik Ulfhammer (1)
  Mia Magnusson (1)
  Karin W?hlander (2)
  Lena Karlsson (1)
  Sverker Jern (1) (3)
  
  1. The Wallenberg Laboratory for Cardiovascular Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
  2. CVGI iMed, AstraZeneca R&D, M?lndal, Sweden
  3. The Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska University Hospital, Bruna str?ket 16, SE-413 45, Gothenburg, Sweden
  
• ISSN：1573-742X

文摘

A reduced capacity for acute tissue-type plasminogen activator (t-PA) release is likely to be associated with an impaired endogenous defense against intravascular thrombosis. Efficient approaches to pharmacologically restore a defective t-PA release have been lacking, but recent observations suggest that histone deacetylase inhibitors (HDACis) enhance t-PA production in vitro. HDACis have diverse chemical structures and different HDAC-enzyme sub-class targeting. We here compared the effects of several clinically used HDACis on t-PA production in endothelial cells. Human umbilical vein endothelial cells were exposed to a panel of 11 different HDACis and t-PA mRNA and protein levels were quantified. All HDACis dose-dependently stimulated t-PA mRNA and protein expression with similar maximal efficacy but with different potencies. Already at low concentrations, the majority of inhibitors caused significant and sustained effects on t-PA production. In addition, selected HDACis were capable of normalizing t-PA production when suppressed by the inflammatory cytokine TNF-α. We conclude that HDACis targeting classical HDAC enzymes are powerful inducers of t-PA expression in cultured endothelial cells and could be promising candidates for pharmacological modulation of endogenous fibrinolysis in man.