Oxidized low density lipoproteins induce a pathologic response by retinal pigmented epithelial cells

The accumulation of apolipoprotein B100 lipoproteins in Bruch membrane is an early event thought to promote age-related macular degeneration (AMD). Immunohistochemistry using an anti-oxidized low density lipoprotein antibody on 10 AMD specimens showed staining in Bruch membrane including basal depos...

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Bibliographic Details
Published in:Journal of neurochemistry 2008-05, Vol.105 (4), p.1187-1197
Main Authors: Yamada, Yuko, Tian, Jane, Yang, Yanqin, Cutler, Roy G, Wu, Tinghuai, Telljohann, Richard S, Mattson, Mark P, Handa, James T
Format: Article
Language:English
Subjects:
Adult
age-related macular degeneration
Aged
Aged, 80 and over
Apoptosis
Apoptosis - physiology
Biochemistry
Biological and medical sciences
Cell Line, Transformed
ceramides
cholesterol
Eye and associated structures. Visual pathways and centers. Vision
Female
Fundamental and applied biological sciences. Psychology
Genotype & phenotype
Humans
Lipid Peroxidation - physiology
Lipoproteins, LDL - metabolism
Lipoproteins, LDL - physiology
Low density lipoprotein
Macular degeneration
Macular Degeneration - etiology
Macular Degeneration - metabolism
Macular Degeneration - pathology
Male
Medical sciences
Middle Aged
Neurology
Ophthalmology
oxidized low density lipoproteins
Pigment Epithelium of Eye - metabolism
Pigment Epithelium of Eye - pathology
retinal pigmented epithelium
Retinopathies
Vertebrates: nervous system and sense organs
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Summary:The accumulation of apolipoprotein B100 lipoproteins in Bruch membrane is an early event thought to promote age-related macular degeneration (AMD). Immunohistochemistry using an anti-oxidized low density lipoprotein antibody on 10 AMD specimens showed staining in Bruch membrane including basal deposits, a marker of AMD. To determine whether retinal pigmented epithelial cells develop a pathologic phenotype after interaction with lipoproteins, ARPE-19 cells were exposed to low density lipoproteins (LDL) or oxidized LDLs (oxLDL). Analysis using the Affymetrix U133 Plus 2.0 (Affymetrix, Inc., Santa Clara, CA, USA) gene chip showed physiological and pathological transcriptional responses after LDL and oxLDL treatment, respectively. LDL induced a down-regulation of cholesterol biosynthesis genes while oxLDL induced transcriptional alterations in genes related to lipid metabolism, oxidative stress, inflammation and apoptosis. Electrospray mass spectrometry showed that oxLDL, but not LDL induced large cellular increases of sphingomyelin, ceramides, and cholesteryl esters. With TUNEL labeling, oxLDL caused 14.6% apoptosis compared to
ISSN:0022-3042
1471-4159
DOI:10.1111/j.1471-4159.2008.05211.x