scholarly journals Metformin alleviates oxidative stress‐induced senescence of human lens epithelial cells via AMPK activation and autophagic flux restoration

2021 ◽  
Author(s):  
Mengmeng Chen ◽  
Chunmei Zhang ◽  
Nan Zhou ◽  
Xu Wang ◽  
Dongmei Su ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Autophagic Flux ◽  
Ampk Activation ◽  
Human Lens Epithelial Cells

Mitochondria-Targeted Antioxidant Peptide SS31 Protects Cultured Human Lens Epithelial Cells against Oxidative Stress

2014 ◽  
Vol 40 (8) ◽  
pp. 822-829 ◽  
Author(s):  
Meng Cai ◽  
Jing Li ◽  
Shaofen Lin ◽  
Xiaoyun Chen ◽  
Juan Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Antioxidant Peptide ◽  
Human Lens Epithelial Cells

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 Long Non-Coding RNA H19 Regulates Human Lens Epithelial Cells Function

2018 ◽  
Vol 50 (1) ◽  
pp. 246-260 ◽  
Author(s):  
Xin Liu ◽  
Chang Liu ◽  
Kun Shan ◽  
Shujie Zhang ◽  
Yi Lu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Differentially Expressed ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Double Staining ◽  
Human Lens Epithelial Cells ◽  
And Migration ◽  
Proliferation And Migration

Background/Aims: Age-related cataract (ARC) remains the leading cause of visual impairment among the elderly population. Long non-coding RNAs (lncRNAs) have emerged as potential regulators in many ocular diseases. However, the role of lncRNAs in nuclear ARC, a subtype of ARC, requires further elucidation. Methods: LncRNA sequencing was performed to identify differentially expressed lncRNAs between the capsules of transparent and nuclear ARC lenses. Expression validation was confirmed by qRT-PCR. MTT assay, Calcein-AM and propidium iodide double staining, Rhodamine 123 and Hoechst double staining, EdU and transwell assay were used to determine the role of H19 or miR-675 in the viability, apoptosis, proliferation and migration of primary cultured human lens epithelial cells (HLECs). Bioinformatics and luciferase reporter assays were used to identify the binding target of miR-675. Results: Sixty-three lncRNAs are differentially expressed between the capsules of transparent and nuclear ARC lenses. One top abundantly expressed lncRNA, H19, is significantly up-regulated in the nuclear ARC lens capsules and positively associated with nuclear ARC grade. H19 knockdown accelerates apoptosis development and reduces the proliferation and migration of HLECs upon oxidative stress. H19 is the precursor of miR-675, and a reduction of H19 inhibits miR-675 expression. miR-675 regulates CRYAA expression by targeting the binding site within the 3’UTR. Moreover, miR-675 increases the proliferation and migration while decreasing the apoptosis of HLECs upon oxidative stress. Conclusion: H19 regulates HLECs function through miR-675-mediated CRYAA expression. This finding would provide a novel insight into the pathogenesis of nuclear ARC.

scholarly journals Study of Oxidative Stress in Human Lens Epithelial Cells Exposed to 1.8 GHz Radiofrequency Fields

PLoS ONE ◽  
2013 ◽  
Vol 8 (8) ◽  
pp. e72370 ◽  
Author(s):  
Shuang Ni ◽  
Yibo Yu ◽  
Yidong Zhang ◽  
Wei Wu ◽  
Kairan Lai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Human Lens Epithelial Cells

scholarly journals Effect of thioltransferase on oxidative stress induced by high glucose and advanced glycation end products in human lens epithelial cells

2021 ◽  
Vol 14 (7) ◽  
pp. 965-972
Author(s):  
Qing Liu ◽  
◽  
Hong Yan ◽  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Advanced Glycation End Products ◽  
High Glucose ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Advanced Glycation ◽  
Human Lens Epithelial Cells ◽  
Glycation End Products ◽  
End Products

AIM: To study the effect of thioltransferase (TTase) on oxidative stress in human lens epithelial cells (HLECs) induced by high glucose and advanced glycation end products (AGEs). METHODS: HLECs were treated with 35.5 mmol/L glucose or 1.5 mg/mL AGEs modified bovine serum albumin (AGEs-BSA) as the experimental groups, respectively. Cells were collected at the time point of 1, 2, 3, and 4d. The TTase activity were measured accordingly. TTase mRNA levels were detected by quantitative reverse transcription polymerase chain response (qRT-RCR) and its protein level was detected by Western blot. The siRNA was used to knock down the expression of TTase. The activity of catalase (CAT) and superoxide dismutase (SOD), the content of reactive oxygen species (ROS) and the ratio of oxidized glutathione/total glutathione (GSSG/T-GSH) were assessed in different groups, respectively. RESULTS: The level of TTase mRNA gradually increased and reached the top at 2d, then it decreased to the normal level at 4d, and the TTase activity increased from 2 to 3d in both high glucose and AGEs-BSA groups. The TTase expression elevated from 2d in high glucose group, and it began to rise from 3d in AGEs-BSA group. The activity of CAT and SOD showed a decrease and the content of ROS and the ratio of GSSG/T-GSH showed an increase in high glucose and AGEs-BSA group. These biochemical alterations were more prominent in the groups with TTase siRNA. CONCLUSION: High glucose and AGEs can increase ROS content in HLECs; therefore, it induces oxidative stress. This may result in the decreased GSH and increased GSSG content, impaired activity of SOD and CAT. The up-regulated TTase likely provides oxidation damage repair induced by high glucose and AGEs in the early stage.

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