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J. Biol. Chem., Vol. 281, Issue 10, 6489-6497, March 10, 2006

This Article Full Text Full Text (PDF) All Versions of this Article: 281/10/6489    most recent M508799200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Munteanu, A. Articles by Zingg, J.-M. Search for Related Content PubMed PubMed Citation Articles by Munteanu, A. Articles by Zingg, J.-M. Social Bookmarking                      What's this?

Antagonistic Effects of Oxidized Low Density Lipoprotein and -Tocopherol on CD36 Scavenger Receptor Expression in Monocytes

INVOLVEMENT OF PROTEIN KINASE B AND PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR-^*

Adelina Munteanu, Michele Taddei, Ilaria Tamburini, Ettore Bergamini, Angelo Azzi, and Jean-Marc Zingg¹

From the Institute of Biochemistry and Molecular Medicine, University of Bern, Bühlstrasse 28, 3012 Bern, Switzerland and the Centro di Ricerca di Biologia e Patologia dell'Invecchiamento, Scuola Medica, University of Pisa, Via Roma 55, 56126 Pisa, Italy

Vitamin E deficiency increases expression of the CD36 scavenger receptor, suggesting specific molecular mechanisms and signaling pathways modulated by -tocopherol. We show here that -tocopherol down-regulated CD36 expression (mRNA and protein) in oxidized low density lipoprotein (oxLDL)-stimulated THP-1 monocytes, but not in unstimulated cells. Furthermore, -tocopherol treatment of monocytes led to reduction of fluorescent oxLDL-3,3'-dioctadecyloxacarbocyanine perchlorate binding and uptake. Protein kinase C (PKC) appears not to be involved because neither activation of PKC by phorbol 12-myristate 13-acetate nor inhibition by PKC412 was affected by -tocopherol. However, -tocopherol could partially prevent CD36 induction after stimulation with a specific agonist of peroxisome proliferator-activated receptor- (PPAR; troglitazone), indicating that this pathway is susceptible to -tocopherol action. Phosphorylation of protein kinase B (PKB) at Ser⁴⁷³ was increased by oxLDL, and -tocopherol could prevent this event. Expression of PKB stimulated the CD36 promoter as well as a PPAR element-driven reporter gene, whereas an inactive PKB mutant had no effect. Moreover, coexpression of PPAR and PKB led to additive induction of CD36 expression. Altogether, our results support the existence of PKB/PPAR signaling pathways that mediate CD36 expression in response to oxLDL. The activation of CD36 expression by PKB suggests that both lipid biosynthesis and fatty acid uptake are stimulated by PKB.

Received for publication, August 10, 2005 , and in revised form, December 5, 2005.

^* This work was supported by the Swiss National Science Foundation. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed. Tel.: 41-31-631-4118; Fax: 41-31-631-3737; E-mail: zin34{at}swissonline.ch.

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