NDLI: Pretreatment with proteasome inhibitors protects against oxidative injuries via PPAR -dependent and -independent pathways in ARPE-19 cells.

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Pretreatment with proteasome inhibitors protects against oxidative injuries via PPAR -dependent and -independent pathways in ARPE-19 cells.

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Pretreatment with proteasome inhibitors protects against oxidative injuries via PPAR -dependent and -independent pathways in ARPE-19 cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Qu, Jia Cai, Jingjing Lin, Bing Wu, Meng'ai Wu, Shengzhou Sun, Lin Snider, B. Joy
Description	Author Affiliation: Cai J ( School of Optometry and Ophthalmology and Eye Hospital, Wenzhou Medical College, Zhejiang, People's Republic of China.)
Abstract	PURPOSES: Oxidative processes may play important roles in age-related macular degeneration. Previous studies have suggested that enhancing proteasome activity by pretreatment with low doses of proteasome inhibitors reduces injury from oxidative damage in neuronal cultures. The objective of the current study was to determine whether proteasome inhibitors could ameliorate the toxicity from oxidative stresses in ARPE-19 cells and to dissect the pathways that may mediate these protective effects. METHODS: The toxicity of oxidative stressors menadione (VK3) and 4-hydroxynonenal (4-HNE) and the protective effects of proteasome inhibitors, including MG-132 and clasto-lactacystin-ß-lactone (LA), were studied in ARPE-19 cells. Binding and activation of the peroxisome proliferator-activated receptors (PPARs) family of transcription factors were studied using electrophoretic mobility shift assay (EMSA) and a peroxisome proliferator-activated response element (PPRE)-driven dual-luciferase reporter gene. RESULTS: An 18-hour pretreatment with 30 to 300 nM MG-132 or 300 to 1000 nM LA reduced the toxicity of menadione or 4-HNE in ARPE-19 cells. The protective effects of MG-132 pretreatment were partially reversed by the PPAR antagonist GW6471 but not by the PPARÎ³ antagonist GW9662; in contrast, neither agent reduced the protective effects of LA. MG-132 but not LA induced increased expression of a PPRE-driven luciferase reporter gene in a dose-dependent manner. Nuclear proteins isolated from ARPE-19 cells treated by MG-132 had increased binding to PPRE sequences as measured by EMSA. CONCLUSIONS: Our data suggest that pretreatment with proteasome inhibitors reduces oxidative injury in ARPE-19 cells and that the underlying mechanisms are different for different proteasome inhibitors, with PPAR -dependent effects for MG-132 and PPAR-independent effects for LA.
ISSN	01460404
e-ISSN	15525783
Journal	Investigative Opthalmology & Visual Science
Issue Number	9
Volume Number	53
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2012-08-31
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cysteine Proteinase Inhibitors Therapeutic Use Oxidative Stress Drug Effects Ppar Alpha Metabolism Retinal Pigment Epithelium Aldehydes Toxicity Anilides Pharmacology Cells, Cultured Electrophoretic Mobility Shift Assay Lactones Leupeptins Oxazoles Agonists Antagonists & Inhibitors Tyrosine Analogs & Derivatives Vitamin K 3 Research Support, Non-u.s. Gov't Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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