Complement-Mediated Regulation of Apolipoprotein E in Cultured Human RPE Cells

Yang, Ping; Skiba, Nikolai P.; Tewkesbury, Grace M.; Treboschi, Victoria; Baciu, Peter; Jaffe, Glenn J.

doi:10.1167/iovs.16-20083

Cited by 26 publications

(28 citation statements)

References 69 publications

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“…RPE cells had apical nuclear localization and basal-lateral localization of phalloidin and ZO-1, as previously reported. 19 Donor RPE cells were seeded on collagen-coated 96-well plates or 24-well plates (Corning-Costar Incorporated, Corning, NY, USA) as we have previously described. 20 For all experiments, cells were grown to confluence prior to treatment.…”

Section: Rpe Cell Culture and Treatmentmentioning

confidence: 99%

Resveratrol Protects Against Hydroquinone-Induced Oxidative Threat in Retinal Pigment Epithelial Cells

Neal

Buehne

Besley

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Oxidative stress in retinal pigment epithelial (RPE) cells is associated with agerelated macular degeneration (AMD). Resveratrol exerts a range of protective biologic effects, but its mechanism(s) are not well understood. The aim of this study was to investigate how resveratrol could affect biologic pathways in oxidatively stressed RPE cells. METHODS. Cultured human RPE cells were treated with hydroquinone (HQ) in the presence or absence of resveratrol. Cell viability was determined with WST-1 reagent and trypan blue exclusion. Mitochondrial function was measured with the XFe24 Extracellular Flux Analyzer. Expression of heme oxygenase-1 (HO-1) and glutamate cysteine ligase catalytic subunit was evaluated by qPCR. Endoplasmic reticulum stress protein expression was measured by Western blot. Potential reactions between HQ and resveratrol were investigated using high-performance liquid chromatography mass spectrometry with resveratrol and additional oxidants for comparison. RESULTS. RPE cells treated with the combination of resveratrol and HQ had significantly increased cell viability and improved mitochondrial function when compared with HQtreated cells alone. Resveratrol in combination with HQ significantly upregulated HO-1 mRNA expression above that of HQ-treated cells alone. Resveratrol in combination with HQ upregulated C/EBP homologous protein and spliced X-box binding protein 1. Additionally, new compounds were formed from resveratrol and HQ coincubation. CONCLUSIONS. Resveratrol can ameliorate HQ-induced toxicity in RPE cells through improved mitochondrial bioenergetics, upregulated antioxidant genes, stimulated unfolded protein response, and direct oxidant interaction. This study provides insight into pathways through which resveratrol can protect RPE cells from oxidative damage, a factor thought to contribute to AMD pathogenesis.

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Section: Rpe Cell Culture and Treatmentmentioning

confidence: 99%

Resveratrol Protects Against Hydroquinone-Induced Oxidative Threat in Retinal Pigment Epithelial Cells

Neal

Buehne

Besley

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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“…It was found that C-reactive protein (CRP) levels appear to be higher in AMD patients (Seddon et al, 2004). When the CRP function is blocked, complement attack induces necrotic RPE cell death (Yang et al, 2011). CRP also recruits complement factor H (CFH) to necrotic lesions and blocks release of proinflammatory cytokines.…”

Section: Inflammatory Nature Of Oxidative Stress-induced Rpe Cell mentioning

confidence: 99%

RPE necroptosis in response to oxidative stress and in AMD

Hanus

Anderson

Wang

2015

Ageing Research Reviews

214

183

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Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly. The underlying mechanism of non-neovascular AMD (dry AMD), also named geographic atrophy (GA) remains unclear and the mechanism of retinal pigment epithelial (RPE) cell death in AMD is controversial. We review the history and recent progress in understanding the mechanism of RPE cell death induced by oxidative stress, in AMD mouse models, and in AMD patients. Due to the limitation of toolsets to distinguish between apoptosis and necroptosis (or necrosis), most previous research concludes that apoptosis is a major mechanism for RPE cell death in response to oxidative stress and in AMD. Recent studies suggest necroptosis as a major mechanism of RPE cell death in response to oxidative stress. Moreover, ultrastructural and histopathological studies support necrosis as major mechanism of RPE cells death in AMD. In this review, we discuss the mechanism of RPE cell death in response to oxidative stress, in AMD mouse models, and in human AMD patients. Based on the literature, we hypothesize that necroptosis is a major mechanism for RPE cell death in response to oxidative stress and in AMD.

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“…Another RPE associated factor, Apolipoprotein E (APoE) has been shown to participate in lipid metabolism and neurodegeneration. Complement activation induces ApoE accumulation in RPE cell and ApoE is commonly detected in the RPE and drusen component in AMD [38].…”

Section: Complementmentioning

confidence: 99%