Cyclic adenosine monophosphate induces plasminogen activator inhibitor-1 expression in human mast cells

Biochem Biophys Res Commun. 2010 Oct 1;400(4):569-74. doi: 10.1016/j.bbrc.2010.08.105. Epub 2010 Sep 8.


Plaminogen activator inhibitor-1 (PAI-1), the key physiological inhibitor of the plasmin fibrinolytic system, plays important roles in the pathogenesis of asthma. Mast cells (MCs) are crucial effector cells and a major source of PAI-1 for asthma. Cyclic adenosine monophosphate (cAMP) is the important regulator of MCs; however, its effects on PAI-1 expression in MCs remain unknown. We reported cAMP/protein kinase A pathway positively regulates PAI-1 expression through cAMP-response element binding protein binding to hypoxia response element-1 at -158 to -153bp of human PAI-1 promoter in human MCs. Moreover, cAMP synergistically augments PAI-1 expression with ionomycin- or IgE receptor cross-linking-mediated stimulation.

MeSH terms

  • Asthma / genetics
  • Asthma / metabolism*
  • Calcium / metabolism
  • Cells, Cultured
  • Cyclic AMP / metabolism*
  • Cyclic AMP / pharmacology
  • Cyclic AMP Response Element-Binding Protein / metabolism*
  • Gene Expression Regulation*
  • Humans
  • Mast Cells / metabolism*
  • Plasminogen Activator Inhibitor 1 / genetics*
  • Promoter Regions, Genetic
  • Receptors, IgE / metabolism
  • Response Elements


  • Cyclic AMP Response Element-Binding Protein
  • Plasminogen Activator Inhibitor 1
  • Receptors, IgE
  • SERPINE1 protein, human
  • Cyclic AMP
  • Calcium