The marine n-3 PUFA DHA evokes cytoprotection against oxidative stress and protein misfolding by inducing autophagy and NFE2L2 in human retinal pigment epithelial cells

Johansson, Ida; Monsen, Vivi Talstad; Pettersen, Kristine; Mildenberger, Jennifer; Misund, Kristine; Kaarniranta, Kai; Schønberg, Svanhild Margrethe Arentz; Bjørkøy, Geir

doi:10.1080/15548627.2015.1061170

Cited by 90 publications

(84 citation statements)

References 103 publications

(113 reference statements)

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“…For the high oxidative stress resistance of RPE cells, the transcription factor nuclear factor erythroid 2related factor 2 (NRF2) also plays an important role (Johansson et al 2015;Lambros & Plafker 2016). NRF2 is activated during oxidative stress and controls the expression of a number of phase-II proteins, and FT is one protein among them (Hayes & Dinkova-Kostova 2014).…”

Section: Discussionmentioning

confidence: 99%

Attenuation of iron‐binding proteins in ARPE‐19 cells reduces their resistance to oxidative stress

Karlsson

Kurz

2016

Acta Ophthalmologica

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Section: Discussionmentioning

confidence: 99%

Attenuation of iron‐binding proteins in ARPE‐19 cells reduces their resistance to oxidative stress

Karlsson

Kurz

2016

Acta Ophthalmologica

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“…Along with the short half-life of ROS, their transient production, such as during a NOX-dependent oxidant burst, these mechanisms topographically limit ROS to a specific locale where they can be neutralized if excessive. Oxidative stress induces a cellular antioxidant response, including in RPE cells, which has been linked to activation of autophagy through the p62/Keap1/Nrf2 pathway (Azad et al, 2009; Filomeni et al, 2010; Johansson et al, 2015; Wang et al, 2014a). Autophagy is a protective, homeostatic mechanism designed to remove faulty cellular components including those generated by oxidative damage.…”

Section: How Does the Rpe Protect Itself From Oxidative Stress?mentioning

confidence: 99%

The impact of oxidative stress and inflammation on RPE degeneration in non-neovascular AMD

Datta

Cano

Ebrahimi

et al. 2017

Progress in Retinal and Eye Research

591

487

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The retinal pigment epithelium (RPE) is a highly specialized, unique epithelial cell that interacts with photoreceptors on its apical side and with Bruch’s membrane and the choriocapillaris on its basal side. Due to vital functions that keep photoreceptors healthy, the RPE is essential for maintaining vision. With aging and the accumulated effects of environmental stresses, the RPE can become dysfunctional and die. This degeneration plays a central role in age-related macular degeneration (AMD) pathobiology, the leading cause of blindness among the elderly in western societies. Oxidative stress and inflammation have both physiological and potentially pathological roles in RPE degeneration. Given the central role of the RPE, this review will focus on the impact of oxidative stress and inflammation on the RPE with AMD pathobiology. Physiological sources of oxidative stress as well as unique sources from photo-oxidative stress, the phagocytosis of photoreceptor outer segments, and modifiable factors such as cigarette smoking and high fat diet ingestion that can convert oxidative stress into a pathological role, and the negative impact of impairing the cytoprotective roles of mitochondrial dynamics and the Nrf2 signaling system on RPE health in AMD will be discussed. Likewise, the response by the innate immune system to an inciting trigger, and the potential role of local RPE production of inflammation, as well as a potential role for damage by inflammation with chronicity if the inciting trigger is not neutralized, will be debated.

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“…Similarly, decreased SQSTM1 levels are associated with autophagy activation (Klionsky et al 2016). The upregulation of SQSTM1/p62 has also been associated with increased oxidative stress and inhibition of proteasome activity in RPE cells Wang et al 2014Wang et al , 2016Johansson et al 2015).…”

Section: Discussionmentioning

confidence: 95%

Absence of collagen XVIII in mice causes age-related insufficiency in retinal pigment epithelium proteostasis

et al. 2016

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Collagen XVIII has the structural properties of both collagen and proteoglycan. It has been found at the basement membrane/stromal interface where it is thought to mediate their attachment. Endostatin, a proteolytic fragment from collagen XVIII C-terminal end has been reported to possess anti-angiogenic properties. Age-related vision loss in collagen XVIII mutant mice has been accompanied with a pathological accumulation of deposits under the retinal pigment epithelium (RPE). We have recently demonstrated that impaired proteasomal and autophagy clearance are associated with the pathogenesis of age-related macular degeneration. This study examined the staining levels of proteasomal and autophagy markers in the RPE of different ages of the Col18a1 (-/-) mice. Eyes from 3, 6-7, 10-13 and 18 months old mice were enucleated and embedded in paraffin according to the routine protocol. Sequential 5 μm-thick parasagittal samples were immunostained for proteasome and autophagy markers ubiquitin (ub), SQSTM1/p62 and beclin-1. The levels of immunopositivity in the RPE cells were evaluated by confocal microscopy. Collagen XVIII knock-out mice had undergone age-related RPE degeneration accompanied by an accumulation of drusen-like deposits. Ub protein conjugate staining was prominent in both RPE cytoplasm and extracellular space whereas SQSTM1/p62 and beclin-1 stainings were clearly present in the basal part of RPE cell cytoplasm in the Col18a1 (-/-) mice. SQSTM1/p62 displayed mild extracellular space staining. Disturbed proteostasis regulated by collagen XVIII might be responsible for the RPE degeneration, increased protein aggregation, ultimately leading to choroidal neovascularization.

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The marine n-3 PUFA DHA evokes cytoprotection against oxidative stress and protein misfolding by inducing autophagy and NFE2L2 in human retinal pigment epithelial cells

Cited by 90 publications

References 103 publications

Attenuation of iron‐binding proteins in ARPE‐19 cells reduces their resistance to oxidative stress

Attenuation of iron‐binding proteins in ARPE‐19 cells reduces their resistance to oxidative stress

The impact of oxidative stress and inflammation on RPE degeneration in non-neovascular AMD

Absence of collagen XVIII in mice causes age-related insufficiency in retinal pigment epithelium proteostasis

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