scholarly journals Orai3 exacerbates apoptosis of lens epithelial cells by disrupting Ca 2+ homeostasis in diabetic cataract

2021 ◽  
Vol 11 (3) ◽  
Author(s):  
Yong Wang ◽  
Suwen Bai ◽  
Ru Zhang ◽  
Lin Xia ◽  
Linghui Chen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lens Epithelial Cells ◽  
Diabetic Cataract

Expression of p53 and caspase-8 in lens epithelial cells of diabetic cataract

2014 ◽  
Vol 40 (7) ◽  
pp. 1102-1108 ◽  
Author(s):  
Sung A. Lim ◽  
Choun-Ki Joo ◽  
Man Soo Kim ◽  
Sung Kun Chung
Keyword(s):  
Epithelial Cells ◽  
Lens Epithelial Cells ◽  
Caspase 8 ◽  
Diabetic Cataract

Orai3 exacerbates apoptosis of lens epithelial cells by disrupting calcium homeostasis in diabetic cataract

Toxicon ◽  
2019 ◽  
Vol 158 ◽  
pp. S85
Author(s):  
Yong Wang ◽  
Suwen Bai ◽  
Juan Du ◽  
Lin Xia ◽  
Jizheng Guo ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Calcium Homeostasis ◽  
Lens Epithelial Cells ◽  
Diabetic Cataract

scholarly journals Effects of microRNA-211 on proliferation and apoptosis of lens epithelial cells by targeting SIRT1 gene in diabetic cataract mice

2017 ◽  
Vol 37 (4) ◽  
Author(s):  
Kun Zeng ◽  
Qi-Gao Feng ◽  
Bao-Tao Lin ◽  
Da-Hui Ma ◽  
Chun-Min Liu
Keyword(s):  
Epithelial Cells ◽  
Protein Concentration ◽  
Negative Control ◽  
Lens Epithelial Cells ◽  
Male Mice ◽  
Healthy Male ◽  
Diabetic Cataract ◽  
Apoptosis Index ◽  
Proliferation And Apoptosis ◽  
Sirt1 Gene

Our study aimed at exploring the effects of miR-211 on the proliferation and apoptosis of lens epithelial cells in diabetic cataract mice by targetting NAD+-dependent histone deacetylase sirtulin 1 (SIRT1). Healthy male mice were assigned into normal and diabetic cataract groups. Blood glucose, lens turbidity, and apoptosis were measured. Lens epithelial cells were classified into the normal, blank, negative control (NC), miR-211 mimics, miR-211 inhibitors, siRNA-SIRT1, and miR-211 inhibitors + siRNA-SIRT1 groups. MiR-211, Bcl-2, Bax, p53, and SIRT1 expressions of each group were detected. Cell proliferation, cycle and apoptosis were tested by MTT assay and flow cytometry. MiR-211 can specifically bind to SIRT1 according to the luciferase system. SIRT1 protein concentration was strongly positive in normal mice and weakly positive in diabetic cataract mice. Apoptosis index of diabetic cataract mice was higher than the normal mice. Compared with normal mice, the expressions of miR-211, Bax, and p53 increased in diabetic cataract mice, while the Bcl-2 and SIRT1 expressions decreased. In comparison with the blank and NC groups, the expressions of miR-211, Bax, and p53 increased, while Bcl-2 and SIRT1 expressions decreased, and the proliferation decreased and apoptosis rate increased in the miR-211 mimics and siRNA-SIRT1 groups; the results were contradicting for the miR-211 inhibitor group. MiR-211 could promote apoptosis and inhibit proliferation of lens epithelial cells in diabetic cataract mice by targetting SIRT1.

scholarly journals LncRNA MALAT1 Regulates miR-144-3p to Facilitate Epithelial-Mesenchymal Transition of Lens Epithelial Cells via the ROS/NRF2/Notch1/Snail Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-23
Author(s):  
Wei Ye ◽  
Jiyuan Ma ◽  
Fang Wang ◽  
Tong Wu ◽  
Mengmei He ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
High Glucose ◽  
Epithelial Mesenchymal Transition ◽  
Phase Cell ◽  
Luciferase Reporter ◽  
Lens Epithelial Cells ◽  
Diabetic Cataract ◽  
Mesenchymal Transition ◽  
Nrf2 Expression ◽  
In Cells

Diabetic cataract is a common complication of diabetes. The epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs) is a key event in the development of diabetic cataracts. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been reported to be highly expressed in different tissues of diabetic patients. This study is aimed at investigating the function and mechanism of MALAT1 in the regulation of EMT in human LECs under high glucose conditions. MALAT1, α-smooth muscle actin (α-SMA), fibronectin (FN), and nuclear factor erythroid-derived 2-like 2 (NRF2) were highly expressed in the LECs of diabetic cataract patients and in the human LECs under high glucose conditions; meanwhile, the decreased expressions of E-cadherin and zonula occludens 1 (ZO-1) were detected. Knockdown of MALAT1 could significantly reduce ROS, prevent EMT, arrest S phase cell cycle, and suppress the expression of total NRF2 and its nucleus translocation in LECs. Furthermore, after NRF2 was knocked down, total NRF2, α-SMA, and FN in cells, and NRF2, Notch intracellular domain (NICD), and Snail were decreased in the nucleus. Using bioinformatics methods, we predicted that MALAT1 and NRF2 shared the same microRNA-144-3p (miR-144-3p) combining site. Luciferase reporter coupled with qRT-PCR assays revealed that miR-144-3p was a target of MALAT1, which was confirmed to downregulate miR-144-3p in the LECs. In addition, after transfection of miR-144-3p mimics or inhibitor, western blot assay demonstrated that miR-144-3p negatively regulated the expression of total NRF2, α-SMA, and FN in cells, and NRF2, NICD, and Snail in the nucleus without affecting Kelch-like ECH-associated protein 1 (KEAP1). Finally, we confirmed that transfection of shMALAT1 inhibited NRF2 expression, and its mediated EMT could be rescued by miR-144-3p inhibitor; transfection of pcDNA3.1-MALAT1 promoted NRF2 expression, and its mediated EMT could be reversed by miR-144-3p inhibitor. In summary, we demonstrate that MALAT1 regulates miR-144-3p to facilitate EMT of LECs via the ROS/NRF2/Notch1/Snail pathway.

scholarly journals AKR1B1-Induced Epithelial–Mesenchymal Transition Mediated by RAGE-Oxidative Stress in Diabetic Cataract Lens

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 273 ◽  
Author(s):  
Tsung-Tien Wu ◽  
Ying-Ying Chen ◽  
Hui-Yu Chang ◽  
Ya-Hsin Kung ◽  
Ching-Jiunn Tseng ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Immunofluorescent Staining ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Cataract Formation ◽  
Diabetic Cataract ◽  
Mesenchymal Transition ◽  
Pharmacological Prevention ◽  
Glycation End Products

Purpose: Cataracts are a major cause of visual acuity deterioration in diabetes mellitus (DM) in developed and developing countries. Studies have demonstrated that overproduction of AKR1B1 and receptor for advanced glycation end products (RAGE) plays a major role in the pathogenesis of diabetic cataracts, but it is unclear whether the prevalence of diabetic cataracts is related to epithelial–mesenchymal transition (EMT) in lens epithelial cells. This study aimed to analyze the role of EMT in cataract formation of DM patients. Methods: Immunofluorescence and immunohistochemistry assays were used to estimate AKR1B1, RAGE, AMPK, and EMT levels in epithelial human lens of DM or non-DM cataracts. Results: Immunohistochemical staining demonstrated that pathologic phases and N-cadherin expression levels were significantly higher in epithelial human lens of DM (+) compared to DM (−) cataracts. Immunofluorescent staining showed that AKR1B1 and RAGE were significantly higher in epithelial human lens of DM (+) compared to DM (−) cataracts. Interestingly, acetyl superoxide dismutase 2 (AcSOD2) levels were significantly higher in DM patients’ lens epithelial cells (LECs), whereas AMPKT172 phosphorylation was significantly increased in non-DM patients. This indicates that AMPKT172 might be related to superoxide reduction and diabetic cataract formation. Conclusions: Our results suggest that AKR1B1 overexpression can decrease AMPK activation, thereby increasing AcSOD2 and RAGE-induced EMT in epithelial human lens of DM cataracts. These novel findings suggest that AKR inhibitors may be candidates for the pharmacological prevention of cataracts in patients with DM.

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