Difference between revisions of "Namgaladze 2010 Atherosclerosis"
Line 11: | Line 11: | ||
{{Labeling | {{Labeling | ||
|organism=Human | |organism=Human | ||
|tissues=Blood | |tissues=Blood cells | ||
|preparations=Intact cells | |preparations=Intact cells | ||
|injuries=RONS; Oxidative Stress, Cancer; Apoptosis; Cytochrome c | |injuries=RONS; Oxidative Stress, Cancer; Apoptosis; Cytochrome c | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} |
Revision as of 09:03, 9 August 2013
Namgaladze D, Preiss S, Dröse S, Brandt U, Brüne B (2010) Phospholipase A2-modified low density lipoprotein induces mitochondrial uncoupling and lowers reactive oxygen species in phagocytes. Atherosclerosis 208: 142-147. |
Namgaladze D, Preiss S, Droese S, Brandt U, Bruene B (2010) Atherosclerosis
Abstract: Low density lipoprotein modified by secretory phospholipase A2 (PLA-LDL) protects monocytes against´oxidative stress. In this study we investigated possible direct effects of PLA-LDL on mitochondrial membrane potential and reactive oxygen species generation. Mitochondrial membrane potential in human monocytic THP-1 cells or primary human monocytes was monitored by flow cytometry using the fluorescent dye 5,5',6,6'-tetrachloro-1,1',3,3'- tetraethylbenzimidazolylcarbocyanine iodide or respirometry. Formation of reactive oxygen species was determined by flow cytometric measuring 2',7'-dichlorofluorescin oxidation. Cell death was assessed using Annexin V/propidium iodide staining. We observed that PLA-LDL caused mitochondrial uncoupling in monocyte/macrophage cell lines as well as in primary human monocytes. PLA-LDL-associated non-esterified fatty acids provoked uncoupling. Uncoupling attenuated reactive oxygen species formation induced by hydrogen peroxide, 2,3-dimethoxy-1,4-naphthoquinone or oxidized LDL. Knock-down of uncoupling protein UCP2 affected neither PLA-LDL-induced uncoupling, nor reactive oxygen species generation. Furthermore,we observed that the chemical uncoupler carbonyl cyanide m-chlorophenylhydrazone increased THP-1 cell survival after hydrogen peroxide treatment. Thus, PLA-LDL-induced uncoupling attenuates reactive oxygen species generation, which may contribute to increased monocyte survival in atherosclerotic plaques and support pro-atherogenic effects of LDL modified by PLA2. • Keywords: Atherosclerosis, Phagocytes, Reactive oxygen species, Phospholipase A2, LDL, Human monocytic THP-1 cells, Primary human monocytes
• O2k-Network Lab: DE_Frankfurt_Brandt U, DE Frankfurt Droese S
Labels:
Stress:RONS; Oxidative Stress"RONS; Oxidative Stress" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property., Cancer; Apoptosis; Cytochrome c"Cancer; Apoptosis; Cytochrome c" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Human Tissue;cell: Blood cells Preparation: Intact cells
HRR: Oxygraph-2k