Regulation of KLF2 Expression by Statins

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Statins, which are the most commonly prescribed class of lipid-lowering agents and were originally designed as inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A, have recently been discovered also to upregulate KLF2 expression in cultured human endothelial cells at pharmacologically relevant doses in vitro (Fig. 4; Parmar et al. 2005b; Sen-Banerjee et al. 2005). Statins block the production of mevalonate, which forms two major downstream products known as isoprenoids: farnesyl pyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP). Both of these isoprenoids can prenylate distinct sets of proteins in the cell to enable their proper localisation and signalling. The statin-mediated upregulation of KLF2 in human umbilical vein endothelial cells (HUVECs) is dependent on the depletion of GGPP (Parmar et al. 2005b; Sen-Banerjee et al. 2005), which is well known to prenylate several members of the Rho superfam-ily. Importantly, upregulation of KLF2 is critical for many statin-dependent transcriptional changes in endothelial cells, thus implicating KLF2 in the so call "pleiotropic" beneficial cardiovascular effects of this class of cardiovascular drugs (Liao and Laufs 2005).

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