Editor's Highlight: Periodic Exposure to Smartphone-Mimic Low-Luminance Blue Light Induces Retina Damage Through Bcl-2/BAX-Dependent Apoptosis

Lin, Cheng Hui; Wu, Man; Li, Ching Hao; Cheng, Hui; Huang, Shu-Hsien; Tsai, Chi Hao; Lin, Fan Li; Ho, Jau Der; Kang, Jaw Jou; Hsiao, George; Cheng, Yu Wen

doi:10.1093/toxsci/kfx030

Cited by 47 publications

(35 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…3A). Moreover, BLL downregulated the protein expression of procaspase-3 and procaspase-8, resulting in more cleavage forms of caspase-3 and caspase-8 after BLL exposure, which is consistent with our previous study [19]. To evaluate the protective effects of CTE further, different concentrations of CTE were applied to BLL-exposed RPE cells (Fig.…”

Section: Cte Inhibits Bll-induced Apoptosis In Rpe Cells By Regulatinsupporting

confidence: 89%

“…Previously, we found that low-intensity long-term BLL exposure induces retinopathy in a rat model [19]; as a continuation of that study, we orally administered CTE to BN rats. BL-induced retinal degeneration and damage has been studied in other models [37,38].…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 86%

“…The light source and cell plates were placed 25 cm apart, as described in our previous study [19]. Luminance was measured with a light meter (LM-81LX; Lutron Electronic Enterprise, Taipei, Taiwan).…”

Section: In Vitro Bl Exposure Protocolmentioning

confidence: 99%

“…We used a periodic low-luminance long-term BLL exposure-induced model of retinal degeneration, as described in our previous study [19]. Briefly, BN rats were divided into three groups: a control group, which was kept under dark conditions; a BLL-exposed group, which was exposed to periodic BLL in the dark without pupil dilation (460 nm, 150 lux) for 3 h per day for 60 days; and a CTE-treated plus BLL-exposed group, which was pre-treated with CTE (100 mg/kg body weight) for 14 days and then co-treated with periodic BLL exposure for 3 h per day for 60 days.…”

Section: Bll-induced Rat Model Of Retinal Degenerationmentioning

confidence: 99%

See 3 more Smart Citations

Novel Protective Effects of Cistanche Tubulosa Extract Against Low-Luminance Blue Light-Induced Degenerative Retinopathy

Lin

et al. 2018

Cell Physiol Biochem

Self Cite

View full text Add to dashboard Cite

Background/Aims: Blue light-emitting diode light (BLL)-induced phototoxicity plays an important role in ocular diseases and causes retinal degeneration and apoptosis in human retinal pigment epithelial (RPE) cells. Cistanche tubulosa extract (CTE) is a traditional Chinese medicine with many beneficial protective properties; however, few studies have examined the ocular protective roles of CTE. In this study, we investigated the mechanisms underlying the effects of CTE on BLL-induced apoptosis in vitro and in vivo. Methods: RPE cells were applied in the current in vitro study and cell viability was determined by an 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Apoptosis-related protein expression was determined by western blot analysis and immunofluorescence staining. Brown Norway rats were used to examine exposure to commercially available BLL in vivo. Hematoxylin and eosin staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and western blot assays were used to examine retinal morphological deformation. Results: CTE significantly inhibited hydrogen peroxide-, tert-butyl hydroperoxide-, sodium azide-, and BLL-induced RPE damage. Further, CTE reduced the expression of apoptotic markers such as cleaved caspase-3 and TUNEL staining after BLL exposure by inactivating apoptotic pathways, as shown via immunofluorescent staining. In addition, CTE inhibited the BLL-induced phosphorylation of c-Jun N-terminal kinase, extra signal-related kinases 1/2, and p38 in RPE cells. In vivo, the oral administration of CTE rescued 60-day periodic BLL exposure-induced decrements in retinal thickness and reduced the number of TUNEL-positive cells in the brown Norway rat model. Conclusion: CTE is a potential prophylactic agent against BLL-induced phototoxicity.

show abstract

Section: Cte Inhibits Bll-induced Apoptosis In Rpe Cells By Regulatinsupporting

confidence: 89%

Section: Cellular Physiology and Biochemistrymentioning

confidence: 86%

Section: In Vitro Bl Exposure Protocolmentioning

confidence: 99%

Section: Bll-induced Rat Model Of Retinal Degenerationmentioning

confidence: 99%

See 2 more Smart Citations

Novel Protective Effects of Cistanche Tubulosa Extract Against Low-Luminance Blue Light-Induced Degenerative Retinopathy

Lin

et al. 2018

Cell Physiol Biochem

Self Cite

View full text Add to dashboard Cite

show abstract

“…In real life, one source of blue light is digital screens. Studies have suggested that periodic exposure to smartphone‐like low‐luminance blue light induces photoreceptor atrophy, decreases retinal thickness, and injures neuron transduction in the retina . Additionally, the RPE cells of STGD1 patients with higher oxygen uptake and light absorption by lipofuscin granules are more susceptible to photo‐oxidative stress than age‐matched controls …”

Section: Introductionmentioning

confidence: 99%

Fundus autofluorescence, spectral‐domain optical coherence tomography, and histology correlations in a Stargardt disease mouse model

et al. 2020

View full text Add to dashboard Cite

Stargardt disease (STGD1), known as inherited retinal dystrophy, is caused by ABCA4 mutations. The pigmented Abca4−/− mouse strain only reflects the early stage of STGD1 since it is devoid of retinal degeneration. This blue light‐illuminated pigmented Abca4−/− mouse model presented retinal pigment epithelium (RPE) and photoreceptor degeneration which was similar to the advanced STGD1 phenotype. In contrast, wild‐type mice showed no RPE degeneration after blue light illumination. In Abca4−/− mice, the acute blue light diminished the mean autofluorescence (AF) intensity in both fundus short‐wavelength autofluorescence (SW‐AF) and near‐infrared autofluorescence (NIR‐AF) modalities correlating with reduced levels of bisretinoid‐fluorophores. Blue light‐induced RPE cellular damage preceded the photoreceptors loss. In late‐stage STGD1‐like patient and blue light‐illuminated Abca4−/− mice, lipofuscin and melanolipofuscin granules were found to contribute to NIR‐AF, indicated by the colocalization of lipofuscin‐AF and NIR‐AF under the fluorescence microscope. In this mouse model, the correlation between in vivo and ex vivo assessments revealed histological characteristics of fundus AF abnormalities. The flecks which are hyper AF in both SW‐AF and NIR‐AF corresponded to the subretinal macrophages fully packed with pigment granules (lipofuscin, melanin, and melanolipofuscin). This mouse model, which has the phenotype of advanced STGD1, is important to understand the histopathology of Stargardt disease.

show abstract

Polydopamine Nanoparticles as Mimicking RPE Melanin for the Protection of Retinal Cells Against Blue Light‐Induced Phototoxicity

Kwon,

Munsoor,

Kaufmann

et al. 2024

Advanced Science

View full text Add to dashboard Cite

Exposure of the eyes to blue light can induce the overproduction of reactive oxygen species (ROS) in the retina and retinal pigment epithelium (RPE) cells, potentially leading to pathological damage of age‐related macular degeneration (AMD). While the melanin in RPE cells absorbs blue light and prevents ROS accumulation, the loss and dysfunction of RPE melanin due to age‐related changes may contribute to photooxidation toxicity. Herein, a novel approach utilizing a polydopamine‐replenishing strategy via a single‐dose intravitreal (IVT) injection is presented to protect retinal cells against blue light‐induced phototoxicity. To investigate the effects of overexposure to blue light on retinal cells, a blue light exposure Nrf2‐deficient mouse model is created, which is susceptible to light‐induced retinal lesions. After blue light irradiation, retina degeneration and an overproduction of ROS are observed. The polydopamine‐replenishing strategy demonstrated effectiveness in maintaining retinal structural integrity and preventing retina degeneration by reducing ROS production in retinal cells and limiting the phototoxicity of blue light exposure. These findings highlight the potential of polydopamine as a simple and effective replenishment for providing photoprotection against high‐energy blue light exposure.

show abstract

Editor's Highlight: Periodic Exposure to Smartphone-Mimic Low-Luminance Blue Light Induces Retina Damage Through Bcl-2/BAX-Dependent Apoptosis

Cited by 47 publications

References 34 publications

Novel Protective Effects of Cistanche Tubulosa Extract Against Low-Luminance Blue Light-Induced Degenerative Retinopathy

Novel Protective Effects of Cistanche Tubulosa Extract Against Low-Luminance Blue Light-Induced Degenerative Retinopathy

Fundus autofluorescence, spectral‐domain optical coherence tomography, and histology correlations in a Stargardt disease mouse model

Polydopamine Nanoparticles as Mimicking RPE Melanin for the Protection of Retinal Cells Against Blue Light‐Induced Phototoxicity

Contact Info

Product

Resources

About