| Oxidative stress increases HO-1 expression in ARPE-19 cells, but melanosomes suppress the increase when light is the stressor. | |
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MedLine Citation:
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PMID: 23221079 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE: Phagocytized melanosomes in ARPE-19 cells were previously shown to decrease susceptibility to oxidative stress induced by hydrogen peroxide treatment and increase stress due to light irradiation relative to cells containing control black latex beads. Here we asked whether differential expression of antioxidant enzymes in cells containing pigment granules could explain the outcomes. METHODS: ARPE-19 cells were loaded by phagocytosis with porcine RPE melanosomes or black latex beads (control particles). Heme oxygenase-1 (HO-1), HO-2, glutathione peroxidase (GPx), and catalase were quantified by Western blot analysis before and after treatment with sublethal hydrogen peroxide or blue light (400-450 nm). The stress was confirmed as sublethal by cell survival analysis using real-time quantification of propidium iodide fluorescence. RESULTS: Phagocytosis itself produced transient changes in protein levels of some antioxidant enzymes, but steady-state levels (7 days after phagocytosis) did not differ in cells containing melanosomes versus beads. Sublethal stress, induced by either hydrogen peroxide or light, had no effect on catalase or HO-2 in either particle-free or particle-loaded cells. In contrast, HO-1 protein was upregulated by treatment with both hydrogen peroxide and light. Particle content did not affect the HO-1 increase induced by hydrogen peroxide, but the increase induced by blue light irradiation was partially blocked in cells containing black beads and blocked even more in cells containing melanosomes. CONCLUSIONS: The results do not implicate differential antioxidant enzyme levels in stress protection by melanosomes against hydrogen peroxide, but they suggest a multifaceted role for melanosomes in regulating light stress susceptibility in RPE cells. |
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Authors:
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Anna Pilat; Anja M Herrnreiter; Christine M B Skumatz; Tadeusz Sarna; Janice M Burke |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2013-01-07 |
Journal Detail:
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Title: Investigative ophthalmology & visual science Volume: 54 ISSN: 1552-5783 ISO Abbreviation: Invest. Ophthalmol. Vis. Sci. Publication Date: 2013 Jan |
Date Detail:
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Created Date: 2013-01-08 Completed Date: 2013-03-05 Revised Date: 2013-04-22 |
Medline Journal Info:
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Nlm Unique ID: 7703701 Medline TA: Invest Ophthalmol Vis Sci Country: United States |
Other Details:
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Languages: eng Pagination: 47-56 Citation Subset: IM |
Affiliation:
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Department of Biophysics, Faculty of Biochemistry, Biophysics, and Biotechnology, Jagiellonian University, Krakow, Poland. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antioxidants / metabolism Cell Line Cell Survival / drug effects, physiology, radiation effects Glutathione Peroxidase / metabolism Heme Oxygenase-1 / metabolism* Humans Hydrogen Peroxide / pharmacology Light Melanosomes / drug effects, metabolism*, radiation effects* Oxidants / pharmacology Oxidative Stress / drug effects, physiology*, radiation effects* Phagocytosis / physiology Retinal Pigment Epithelium* / cytology, metabolism, radiation effects Swine |
| Grant Support | |
ID/Acronym/Agency:
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C06 RR-RR016511/RR/NCRR NIH HHS; P30 EY001931/EY/NEI NIH HHS; P30EY01931/EY/NEI NIH HHS; R01 EY019664/EY/NEI NIH HHS; R01EY019664/EY/NEI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antioxidants; 0/Oxidants; 7722-84-1/Hydrogen Peroxide; EC 1.11.1.-/glutathione peroxidase GPX1; EC 1.11.1.9/Glutathione Peroxidase; EC 1.14.99.3/HMOX1 protein, human; EC 1.14.99.3/Heme Oxygenase-1 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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