Visit our Expo - Redox and Inflammation signaling 2012

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Acute anti-inflammatory properties of statins involve Peroxisome Proliferator-Activated Receptor-alpha via inhibition of the PKC signalling pathway Réjane Paumelle 1 , Christophe Blanquart 1 , Olivier Briand 1 , Olivier Barbier 1 , Gaëtane Woerly 2 Christian Duhem 1 , Frédéric Percevault 1 , Jean-Charles Fruchart 1 , David Dombrowicz 2 , Corine Glineur 1 and Bart Staels 1,3 . 1 Département d’Athérosclerose, U545 Inserm, Institut Pasteur de Lille and Faculté de Pharmacie, Université de Lille II, Lille, France. 2 Inserm U547, Institut Pasteur de Lille, Lille, France. E-mail: Bart.Staels@pasteur-lille.fr Statins are inhibitors of 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase used in the prevention of cardiovascular diseases (CVD). In addition to their cholesterol-lowering activities, statins exert pleiotropic anti-inflammatory effects, which might contribute to their beneficial effects not only on CVD, but also on lipid-unrelated immune and inflammatory diseases, such as rheumatoid arthritis, asthma, stroke and transplant rejection. However, the molecular mechanisms involved in these anti-inflammatory properties of statins are unresolved. The nuclear receptor Peroxisome Proliferator-Activated Receptor (PPAR)-alpha that is expressed in inflammation regulatory cell types, such as macrophages, exerts potent anti-inflammatory activities. In this study we present genetic evidence for a role for this nuclear receptor in mediating the lipid-independent anti-inflammatory activities of statins in two in vivo models of acute inflammation. Furthermore, the inhibitory effects of statins on lipopolysaccharide (LPS)-induced inflammatory response genes were abolished in PPARalpha-deficient macrophages and neutrophils, two cell types involved in acute inflammatory responses. Moreover, we provide a molecular mechanism explaining these observations by showing that simvastatin inhibited PPAR-alpha phosphorylation by LPS-activated PKCalpha. A constitutive active form of PKC-alpha inhibited NF-kappaB transrepression by PPAR-alpha whereas simvastatin enhanced transrepression activity of wild-type PPAR-alpha, but not of PPAR-alpha mutated in its PKC phosphorylation sites. These data indicate that the acute anti-inflammatory effect of simvastatin occurs via PPAR-alpha by a mechanism involving inhibition of PKC-alpha inactivation of PPAR-alpha transrepression activity. PUBLICATIONS - Tulasne, D., Paumelle, R., Weidner, M., Vandenbunder, B. and Fafeur, V. The multisubstrate docking site of the MET receptor is dispensable for MET-mediated RAS signaling and cell scattering. 1999. Mol. Biol. Cell. 10, 551-565. - Paumelle, R., Tulasne, D., Leroy, C., Coll, J., Vandenbunder, B. and Fafeur, V. Sequential activation of ERK and repression of JNK by SF/HGF in MDCK epithelial cells. 2000. Mol. Biol. Cell. 11, 3751-3763. - Paumelle, R., Tulasne, D., Kherrouche, Z., Plaza, S., Leroy, C., Reveneau, S., Vandenbunder, B. And Fafeur, V. Hepatocyte growth factor/scatter factor activates the ETS1 transcription factor by a RAS-RAF-MEK-ERK signaling pathway. 2002. Oncogene. 21: 2309-2319. - Blanquart, C., Mansouri, R., Paumelle, R., Fruchart, J. C., Staels, B. The protein kinase C signalling pathway regulates a molecular switch between transactivation and transrepression - 78 -
activity of the Peroxisome Proliferator-Activated Receptor alpha (PPAR{alpha}). 2004. Mol Endocrinol.18(8):1906-18. -Teissier, E., Nohara, A., Chinetti, G., Paumelle, R., Cariou, B., Fruchart, J.C., Brandes, R., Shah, A., Staels, B. Peroxisome proliferator-activated receptor induces NADPH oxydase activity in macrophages leading to the generation of LDL with PPAR activation properties. 2004. Circ. Res. 95(12):1174-82. - Paumelle, R., Blanquart, C., Briand, O., Barbier, O, Woerly, G, Duhem, C., Percevault, F., Fruchart, J. C., Dombrowicz, D., Glineur, C., and Staels, B. Acute anti-inflammatory properties of statins involve Peroxisome Proliferator-Activated Receptor-alpha via inhibition of the PKC signalling pathway. In revision in Circ. Res. - 79 -
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Table of content PREFACE ..........
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Preface In 1998, we organized the f
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Acknowledgments This meeting has be
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Group B (15h00 - 17h00) Session V.
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Visit our Expo (in alphabetical ord
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Thursday January 26th, 2006 (Early
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Regulation of inflammation and gluc
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Oral presentations (by alphabetical
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4: : Lottin S, Vercoutter-Edouart A
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Session XVII : Cell signaling in he
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Dr. Nassera Aouali L-1526 Luxembour
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Pr. Czeslaw Cierniewski 92-215 Lodz
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Dr. Jochen Hefl Division of Signal
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Mr. Jan Jepsen 2100 Copenhagen DNK
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Pr. Young Min Kim Division of Biolo
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