Title : Inhibitory effect of simvastatin on the TNF-alpha- and angiotensin II-induced monocyte adhesion to endothelial cells is mediated through the suppression of geranylgeranyl isoprenoid-dependent ROS generation.

Pub. Date : 2008 Feb

PMID : 18365690






5 Functional Relationships(s)
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1 Inhibitory effect of simvastatin on the TNF-alpha- and angiotensin II-induced monocyte adhesion to endothelial cells is mediated through the suppression of geranylgeranyl isoprenoid-dependent ROS generation. Simvastatin tumor necrosis factor Homo sapiens
2 Simvastatin, a HMG-CoA reductase inhibitor, suppressed both tumor necrosis factor (TNF)-alpha- and angiotensin (Ang) II-induced monocyte adhesion to endothelial cells (an initial step in vascular inflammation) and reactive oxygen species (ROS) production. Simvastatin tumor necrosis factor Homo sapiens
3 Furthermore, exogenously applied mevalonate or geranylgeranylpyrophosphate in combination with simvastatin completely prevented the inhibitory effects of simvastatin on ROS generation and monocyte-endothelial cell adhesion by TNFalpha and Ang II. Simvastatin tumor necrosis factor Homo sapiens
4 Furthermore, exogenously applied mevalonate or geranylgeranylpyrophosphate in combination with simvastatin completely prevented the inhibitory effects of simvastatin on ROS generation and monocyte-endothelial cell adhesion by TNFalpha and Ang II. Simvastatin tumor necrosis factor Homo sapiens
5 These results suggest that monocyte adhesion to endothelial cells induced by TNF-alpha or Ang II is mediated via the geranylgeranyl isoprenoid-dependent generation of ROS, and that this is inhibited by simvastatin. Simvastatin tumor necrosis factor Homo sapiens