Pitavastatin suppresses mitogen activated protein kinase-mediated Erg-1 induction in human vascular smooth muscle cells Academic Article uri icon


MeSH Major

  • Early Growth Response Protein 1
  • MAP Kinase Signaling System
  • Mitogen-Activated Protein Kinases
  • Muscle, Smooth, Vascular
  • Quinolines
  • Transcriptional Activation


  • Statins have been demonstrated to elicit a broad range of cellular events resulting in an attenuation of the inflammatory response and enhanced protection to the components of the vessel wall. The present study was designed to examine the effect of pitavastatin on pathways associated with the proinflammatory gene, early growth response (Egr)-1, in human vascular smooth muscle cells. Pretreatment with pitavastatin resulted in a dose-dependent reduction in Egr-1 protein and suppressed Egr-1 mRNA expression in response to phorbol 12-myristate 13-acetate (PMA). A reduction in Egr-1 expression reduced the activation of NGFI-A binding protein (NAB)-2, an Egr-1-dependent gene. Furthermore, these events appeared to be dependent on the ability of pitavastatin to attenuate signaling cascades associated with extracellular regulated kinase (ERK) 1/2, but not p38 and c-Jun N-terminal kinase (JNK).

publication date

  • March 15, 2009



  • Academic Article



  • eng

PubMed Central ID

  • PMC2671580

Digital Object Identifier (DOI)

  • 10.1016/j.ejphar.2008.12.047

PubMed ID

  • 19374880

Additional Document Info

start page

  • 72

end page

  • 6


  • 606


  • 1-3