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Protective effects on age-related macular degeneration by activated autophagy induced by amyloid-β in retinal pigment epithelial cells.

07:00 EST 1st March 2019 | BioPortfolio

Summary of "Protective effects on age-related macular degeneration by activated autophagy induced by amyloid-β in retinal pigment epithelial cells."

Amyloid-β (Aβ) accumulation has been reported in patients with age-related macular degeneration (AMD), and it has been demonstrated to play an important role in the development of AMD. This study was performed to detect the activation of autophagy in retinal pigment epithelial (RPE) cells treated with Aβ, aiming to investigate the potential protective mechanism of RPE cells against Aβ stress. Human ARPE-19 cells were treated with soluble Aβ1-42 oligomer. Transmission electron microscopy was used to assess the formation of autophagic compartments; immunofluorescence was used to detect the subcellular localization of LC3; and western blot was used to detect the conversion of LC3-I to LC3-II and the expression of p62. Activated autophagy in Aβ-treated ARPE-19 cells was detected by three methodologies: 1) generation of autophagic compartments by transmission electron microscopy, 2) altered expression pattern of LC3 by immunofluorescence, and 3) elevated light-chain-3 II (LC3-II) and decreased p62 expression by western blot. These results suggest that Aβ could induce autophagy in RPE cells, which provided a potential protective mechanism for the retina cells that encountered Aβ deposition.

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This article was published in the following journal.

Name: Discovery medicine
ISSN: 1944-7930
Pages: 153-160

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Medical and Biotech [MESH] Definitions

A form of MACULAR DEGENERATION also known as dry macular degeneration marked by occurrence of a well-defined progressive lesion or atrophy in the central part of the RETINA called the MACULA LUTEA. It is distinguishable from WET MACULAR DEGENERATION in that the latter involves neovascular exudates.

An autophagy related protein that is similar to UBIQUITIN-ACTIVATING ENZYME E1. It functions in CYTOPLASM to VACUOLE transport (Cvt) and AUTOPHAGY by activating ATG12 PROTEIN for its conjugation with ATG5 PROTEIN, as well as the conjugation of ATG8 FAMILY PROTEINS with phosphatidylethanolamine for ATG8 association to Cvt vesicles and AUTOPHAGOSOME membranes. It is also required for the nitrogen starvation response in yeast, MITOPHAGY; and autophagic cell death induced by CASPASE 8 inhibition.

Specialized ophthalmic technique used in the surgical repair and or treatment of disorders that include retinal tears or detachment; MACULAR HOLES; hereditary retinal disease; AIDS-related retinal infections; ocular tumors; MACULAR DEGENERATION; DIABETIC RETINOPATHY; and UVEITIS.

A serine/threonine-protein kinase that functions in AUTOPHAGY in response to starvation. It acts on the PHOSPHATIDYLINOSITOL 3-KINASE complex PIK3C3 to regulate AUTOPHAGOSOME formation. It also functions as both a downstream effector and negative regulator of mammalian target of rapamycin complex 1 (mTORC1) and is activated by AMPK, which it also negatively regulates.

A retrogressive pathological change in the retina, focal or generalized, caused by genetic defects, inflammation, trauma, vascular disease, or aging. Degeneration affecting predominantly the macula lutea of the retina is MACULAR DEGENERATION. (Newell, Ophthalmology: Principles and Concepts, 7th ed, p304)

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