scholarly journals Ferulic Acid Suppresses AmyloidβProduction in the Human Lens Epithelial Cell Stimulated with Hydrogen Peroxide

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Noriaki Nagai ◽  
Sachiyo Kotani ◽  
Yu Mano ◽  
Akina Ueno ◽  
Yoshimasa Ito ◽  
...  
Keyword(s):  
Gene Expression ◽  
Ferulic Acid ◽  
Lens Epithelial Cell ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Rt Pcr ◽  
Human Lens Epithelial Cell ◽  
Oxidative Stresses ◽  
Age Related ◽  
The Brain

It is well known that oxidative stresses induce the production of amyloidβ(Aβ) in the brain, lens, and retina, leading to age-related diseases. In the present study, we investigated the effects of ferulic acid on the Aβlevels in H2O2-stimulated human lens epithelial (HLE) SRA 01/04 cells. Three types of Aβpeptides (Aβ1-40, Aβ1-42, and Aβ1-43) were measured by ELISA, and the levels of mRNA for the expressed proteins related to Aβproduction (APP, BACE1, and PS proteins) and degradation (ADAM10, NEP, and ECE1 proteins) were determined by quantitative real-time RT-PCR. H2O2stimulation augmented gene expression of the proteins related to Aβproduction, resulting in the production of three types of Aβpeptides. Treatment with 0.1 μM ferulic acid attenuated the augmentations of gene expression and production of the proteins related to the secretion of three types of Aβpeptides in the H2O2-stimulated HLE cells. These results provided evidence of antioxidative functions of ferulic acid for lens epithelial cells.

Characterization of Zinc Oxide Nanoparticles and their Inhibitory Effect on Human Lens Epithelial Cells under UVB Irradiation

2013 ◽  
Vol 788 ◽  
pp. 61-64
Author(s):  
Da Dong Guo ◽  
Hong Ying Tang ◽  
Hong Sheng Bi
Keyword(s):  
Epithelial Cells ◽  
Zno Nanoparticles ◽  
Lens Epithelial Cell ◽  
Human Lens ◽  
Posterior Capsular Opacification ◽  
Lens Epithelial Cells ◽  
Epithelial Cell Proliferation ◽  
Uvb Irradiation ◽  
Human Lens Epithelial Cell ◽  
Human Lens Epithelial Cells

Posterior capsular opacification is the most frequent complication after cataract surgery, which is induced by the proliferation, differentiation and migration of lens epithelial cells. Inhibiting the proliferation of human lens epithelial cells could reduce the occurrence of posterior capsular opacification. To explore the possible potential of ZnO nanoparticles in treating posterior capsular opacification, we investigated the effect of ZnO nanoparticles on the human lens epithelial cell proliferation in the presence and absence of ultraviolet B (UVB) irradiation via 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay. The results indicate that ZnO nanoparticles could apparently inhibit the proliferation of human lens epithelial cells in a dose-dependent manner, and UVB irradiation can further enhance this inhibitory role for the human lens epithelial cell proliferation, indicating the great potential of ZnO nanoparticles in treating posterior capsular opacification in clinical application.

scholarly journals SUMOylation Evoked by Oxidative Stress Reduced Lens Epithelial Cell Antioxidant Functions by Increasing the Stability and Transcription of TP53INP1 in Age-Related Cataracts

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Bo Lu ◽  
Ian T. Christensen ◽  
Tao Yu ◽  
Chunxia Wang ◽  
Qichang Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Epithelial Cell ◽  
Cell Injury ◽  
Lens Epithelial Cell ◽  
Human Lens ◽  
Human Lens Epithelial Cell ◽  
Age Related ◽  
The Stability

Oxidative stress plays an important role in the pathogenesis of cataracts. Small ubiquitin-like modifier (SUMO) proteins have great effects on cell stress response. Previous studies have shown that TP53INP1 can arrest cell growth and induce apoptosis by modulating p53 transcriptional activity and that both TP53INP1 and p53 are substrates of SUMOylation. However, no previous research has studied the effect of SUMOylation on the oxidative stress response in cataracts. This is the first study to investigate the effect of SUMOylation of TP53INP1 in oxidative stress-induced lens epithelial cell injury and age-related cataract formation. We found that the oxidative stress-induced endogenous SUMOylation of TP53INP1 promoted human lens epithelial cell (holed) apoptosis and regulated hLEC antioxidant effects by increasing the stability and transcription of TP53INP1 in age-related cataracts. SUMO-1, SUMOylation, and TP53INP1 were upregulated in lens tissues affected by age-related cataracts. A SUMO-1-specific protease, SENP1, acted as an oxidative stress-sensitive target gene in hLECs. This study identified for the first time that TP53INP1 can be SUMOylated in vivo, that the SUMOylation of TP53INP1 is induced by oxidative stress, and that SUMOylation/deSUMOylation can affect the stability and transcription of TP53INP1 in hLECs.

scholarly journals Nanoceria Prevents Glucose-Induced Protein Glycation in Eye Lens Cells

Nanomaterials ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1473
Author(s):  
Belal I. Hanafy ◽  
Gareth W. V. Cave ◽  
Yvonne Barnett ◽  
Barbara K. Pierscionek
Keyword(s):  
Protein Glycation ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Oxide Nanoparticles ◽  
Lens Protein ◽  
Oxygen Species ◽  
Human Lens Epithelial Cells ◽  
Age Related ◽  
Age Related Changes

Cerium oxide nanoparticles (nanoceria) are generally known for their recyclable antioxidative properties making them an appealing biomaterial for protecting against physiological and pathological age-related changes that are caused by reactive oxygen species (ROS). Cataract is one such pathology that has been associated with oxidation and glycation of the lens proteins (crystallins) leading to aggregation and opacification. A novel coated nanoceria formulation has been previously shown to enter the human lens epithelial cells (HLECs) and protect them from oxidative stress induced by hydrogen peroxide (H2O2). In this work, the mechanism of nanoceria uptake in HLECs is studied and multiple anti-cataractogenic properties are assessed in vitro. Our results show that the nanoceria provide multiple beneficial actions to delay cataract progression by (1) acting as a catalase mimetic in cells with inhibited catalase, (2) improving reduced to oxidised glutathione ratio (GSH/GSSG) in HLECs, and (3) inhibiting the non-enzymatic glucose-induced glycation of the chaperone lens protein α-crystallin. Given the multifactorial nature of cataract progression, the varied actions of nanoceria render them promising candidates for potential non-surgical therapeutic treatment.

EAAT and Xc−Exchanger Inhibition Depletes Glutathione in the Transformed Human Lens Epithelial Cell Line SRA 01/04

2015 ◽  
pp. 1-10 ◽  
Author(s):  
Marlyn P. Langford ◽  
Thomas B. Redens ◽  
Chanping Liang ◽  
A. Scott Kavanaugh ◽  
Donald E. Texada
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Lens Epithelial Cell ◽  
Human Lens ◽  
Epithelial Cell Line ◽  
Human Lens Epithelial Cell

scholarly journals Thioredoxin Binding Protein-2 Regulates Autophagy of Human Lens Epithelial Cells under Oxidative Stress via Inhibition of Akt Phosphorylation

2016 ◽  
Vol 2016 ◽  
pp. 1-17 ◽  
Author(s):  
Jiaojie Zhou ◽  
Ke Yao ◽  
Yidong Zhang ◽  
Guangdi Chen ◽  
Kairan Lai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Cell Viability ◽  
Binding Protein ◽  
Negative Regulator ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Human Lens Epithelial Cells ◽  
Age Related

Oxidative stress plays an essential role in the development of age-related cataract. Thioredoxin binding protein-2 (TBP-2) is a negative regulator of thioredoxin (Trx), which deteriorates cellular antioxidant system. Our study focused on the autophagy-regulating effect of TBP-2 under oxidative stress in human lens epithelial cells (LECs). Human lens epithelial cells were used for cell culture and treatment. Lentiviral-based transfection system was used for overexpression of TBP-2. Cytotoxicity assay, western blot analysis, GFP/mCherry-fused LC3 plasmid, immunofluorescence, and transmission electronic microscopy were performed. The results showed that autophagic response of LECs with increased LC3-II, p62, and GFP/mCherry-LC3 puncta (P<0.01) was induced by oxidative stress. Overexpression of TBP-2 further strengthens this response and worsens the cell viability (P<0.01). Knockdown of TBP-2 attenuates the autophagic response and cell viability loss induced by oxidative stress. TBP-2 mainly regulates autophagy in the initiation stage, which is mTOR-independent and probably caused by the dephosphorylation of Akt under oxidative stress. These findings suggest a novel role of TBP-2 in human LECs under oxidative stress. Oxidative stress can cause cell injury and autophagy in LECs, and TBP-2 regulates this response. Hence, this study provides evidence regarding the role of TBP-2 in lens and the possible mechanism of cataract development.

scholarly journals Let-7c-3p Regulates Autophagy under Oxidative Stress by Targeting ATG3 in Lens Epithelial Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Ting Li ◽  
Yanhong Huang ◽  
Wenkai Zhou ◽  
Qichang Yan
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Western Blot ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Age Related ◽  
Spot Number ◽  
Gene Assay

Background. Oxidative stress is an important factor during age-related cataract formation. Apoptosis and autophagy induced by oxidative stress have been reported as key factors in age-related cataract. In our research, we investigated the role of let-7c-3p in the regulation of autophagy and apoptosis during the formation of age-related cataract. Material and Methods. Real-time PCR and western blot were employed to detect the expression of let-7c-3p in the tissues of age-related cataract. Human lens epithelial cells (LECs) were treated with H2O2 as an age-related cataract model. The extent of apoptosis was measured by flow cytometry and western blot. To detect autophagy, immunofluorescence was used to analyze the spot number of LC3, and western blot was used to detect the expression of LC3-II/I and ATG3. The molecular mechanisms of let-7c-3p regulating autophagy via ATG3 under oxidative stress were performed by a luciferase report gene assay and rescue experiment. Results. Downregulation of let-7c-3p was found in the age-related cataract group aged >65 years relative to the age-related cataract group aged ≤65 years. Consistently, the expression of let-7c-3p was also lower under oxidative stress. The activities of LEC apoptosis and autophagy induced by oxidative stress were inhibited by let-7c-3p. By the bioinformatics database and the luciferase reporter assay, ATG3 was found to be a direct target of let-7c-3p. Let-7c-3p reduced the ATG3-mediated autophagy level, which was induced by oxidative stress in LECs. Conclusion. Let-7c-3p inhibits autophagy by targeting ATG3 in LECs in age-related cataract.

Sign in / Sign up

Export Citation Format

Share Document