Literature DB >> 19595352

Lovastatin inhibits oxidized L-A-phosphatidylcholine B-arachidonoyl-gamma-palmitoyl (ox-PAPC)-stimulated interleukin-8 mRNA and protein synthesis in human aortic endothelial cells by depleting stores of geranylgeranyl pyrophosphate.

Lucas A Dvoracek1, Jeffrey I Kreisberg, Jordan McKinney, Gabrielle Schmid, Amanda D Francis, Katie L Kacmarik, Huey Miin Lee, Melinda S Detrick, Donald A Primerano, Nalini Santanam, Robert Kreisberg.   

Abstract

Human aortic endothelial cells (HAEC) exposed to 50 microg/ml oxidized L-A-phosphatidylcholine B-arachidonoyl-gamma-palmitoyl (ox-PAPC) for 6h increased in interleukin-8 mRNA and protein levels. Preincubation of HAEC with the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG CoA) inhibitor, (20 microM), significantly inhibited ox-PAPC-stimulated interleukin-8 mRNA and protein levels. Mevalonate (200 microM) reversed the inhibition of ox-PAPC-stimulated mRNA and protein levels by lovastatin, indicating the inhibitory effect of lovastatin was due to inhibition of mevalonate synthesis. Addition of the geranylgeraniol (GGOL, 10 microM) but not farnesol (FOL, 10 microM), reversed the inhibitory effect of lovastatin on interleukin-8 mRNA and protein levels stimulated by ox-PAPC, indicating that lovastatin exerted its effect by inhibiting stores of geranylgeranyl pyrophosphate (GGPP) which are necessary for geranylgeranylation of proteins. These results suggest a new mechanism for lovastatin in preventing atherosclerosis by inhibiting the inflammatory response that takes place in the vascular wall. Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.

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Year:  2009        PMID： 19595352      PMCID： PMC2813419          DOI： 10.1016/j.atherosclerosis.2009.06.013

Source DB:  PubMed          Journal:  Atherosclerosis        ISSN： 0021-9150            Impact factor:   5.162


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