J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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A more recent version of this article appeared on January 1, 2008

Papers In Press, published online ahead of print September 21, 2007
J. Lipid Res., doi:10.1194/jlr.M700100-JLR200
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Submitted on February 27, 2007
Revised on September 18, 2007
Accepted on September 21, 2007

Oxidized LDL attenuates apoptosis in monocytic cells by activating ERK signaling

Dmitry Namgaladze, Andreas Kollas, and Bernhard Brüne

Institute Biochemistry I - Pathobiochemistry, Johann Wolfgang Goethe-University, Frankfurt am Main 60596

Corresponding Author: bruene{at}zbc.kgu.de

Low concentrations of oxidized low density lipoprotein (oxLDL) are cytoprotective for phagocytes, although underlying mechanisms remain unclear. We investigated signaling pathways used by oxLDL to attenuate apoptosis in monocytic cells. oxLDL at 25-50 µg/ml inhibited staurosporine-induced apoptosis in THP-1 cells and mouse peritoneal macrophages, and it was cytoprotective in human primary monocytes upon serum withdrawal. Attenuated cell demise was reversed by blocking ERK signaling. Translocation of cytochrome c to the cytosol was attenuated by oxLDL, which again demanded ERK-signaling. Analysis of Bcl-2 family proteins revealed phosphorylation of Bad at S112 as well as ERK-dependent inhibition of Mcl-1 degradation. Although formation of reactive oxygen species (ROS) is an established signal generated by oxLDL, ROS scavengers did not interfere with cell protection by oxLDL. Thus, activation of the ERK signaling pathway by oxLDL is important to protect phagocytes from apoptosis.


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[Abstract] [Full Text] [PDF]


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