Application of Saturation Dye 2D-DIGE Proteomics to Characterize Proteins Modulated by Oxidized Low Density Lipoprotein Treatment of Human Macrophages

2008 ◽  
Vol 7 (8) ◽  
pp. 3572-3582 ◽  
Author(s):  
Annabelle Dupont ◽  
Maggy Chwastyniak ◽  
Olivia Beseme ◽  
Anne-Laure Guihot ◽  
Hervé Drobecq ◽  
...  
Blood ◽  
2003 ◽  
Vol 101 (12) ◽  
pp. 4847-4849 ◽  
Author(s):  
Vladimir A. Shatrov ◽  
Vadim V. Sumbayev ◽  
Jie Zhou ◽  
Bernhard Brüne

Abstract Oxidized low-density lipoprotein (oxLDL) and macrophages play a central role in atherosclerosis. Here, we obtained evidence that oxLDL induced hypoxia-inducible factor-1α (HIF-1α) protein accumulation in human macrophages (Mono-Mac-6) under normoxia. HIF-1α accumulation was attenuated by pretreatment with the antioxidant N-acetyl-L-cysteine (NAC), the nitric oxide (NO) donor S-nitrosoglutathione (GSNO), and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitors such as diphenyleniodonium (DPI) or 4-(2-aminoethyl)-benzenesulfonyl fluoride (AEBSF), thus implicating the contribution of oxLDL-generated reactive oxygen species (ROS). Whereas oxLDL did not modulate HIF-1α mRNA levels, experiments with cycloheximide pointed to a translational mechanism in oxLDL action. HIF-1–dependent luciferase reporter gene analysis underscored HIF-1 transactivation. Our results indicate that oxLDL induced HIF-1α accumulation and HIF-1–dependent reporter gene activation in human macrophages via a redox-mediated pathway. This finding may suggest a role of HIF-1 in atherosclerosis and oxLDL-induced pathogenesis.


Author(s):  
Ekaterina V. Nekrasova ◽  
Ekaterina E. Larionova ◽  
Katerina Danko ◽  
Darya O. Kuzmina ◽  
Vladimir S. Shavva ◽  
...  

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