miR-211 promotes lens epithelial cells apoptosis by targeting silent mating-type information regulation 2 homolog 1 in age-related cataracts.

Int J Ophthalmol

Department of Ophthalmology, the Fourth Affiliated Hospital of China Medical University, Key Laboratory of Lens Research of Liaoning Province, Eye Hospital of China Medical University, Shenyang 110005, Liaoning Province, China.

Published: February 2018

Aim: To detect the expression of miR-211 in age-related cataract tissue, explore the effects of miR-211 on lens epithelial cell proliferation and apoptosis, and identify its target gene.

Methods: This study used real-time quantitative polymerase chain reaction (RT-qPCR) to measure the expression of miR-211 and its predicted target gene [silent mating-type information regulation 2 homolog 1 (SIRT1)] in 46 anterior lens capsules collected from age-related cataract patients. Human lens epithelial cell line (SRA01/04) cells were transfected with either miR-211 mimics, mimic controls, miR-211 inhibitors or inhibitor controls, 72h after transfection, miRNA and protein expression of SIRT1 were measured using RT-qPCR and Western blotting; then cells were exposed to 200 µmol/L HO for 1h, whereupon cell viability was measured by MTS assay, caspase-3 assay was performed. Dual luciferase reporter assay was performed to verify the relationship between miR-211 of SIRT1.

Results: Compared to the control group, expression of miR-211 was significantly increased (<0.001), the miRNA and protein expression of SIRT1 were significantly decreased (<0.001) in the anterior lens capsules of patients with age-related cataracts. Relative to the control group, SIRT1 miRNA and protein levels in the miR-211 mimic group were significantly reduced, cell proliferation activity significantly decreased, and caspase-3 activity was significantly increased (<0.001). In the miR-211 inhibitor group, SIRT1 miRNA and protein expression were significantly increased, cell proliferation activity significantly increased, and caspase-3 activity was significantly decreased (<0.001). A dual luciferase reporter assay confirmed that SIRT1 is a direct target of miR-211.

Conclusion: miR-211 is highly expressed in the anterior lens capsules of patients with age-related cataracts. By negatively regulating the expression of SIRT1, miR-211 promotes lens epithelial cell apoptosis and inhibits lens epithelial cell proliferation.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5824072PMC
http://dx.doi.org/10.18240/ijo.2018.02.04DOI Listing

Publication Analysis

Top Keywords

lens epithelial
12
expression mir-211
12
mir-211
8
mating-type regulation
8
regulation homolog
8
age-related cataract
8
epithelial cell
8
assay performed
8
mir-211 promotes
4
lens
4

Similar Publications

SP1/COL1A2/ZEB1 axis promotes TGF-β2-induced lens epithelial cell proliferation, migration, invasion and EMT process.

Exp Eye Res

December 2024

Department of Ophthalmology, Shaanxi Eye Hospital, Xi'an People's Hospital (Xi'an Fourth Hospital), Affiliated People's Hospital of Northwest University, Xi'an 710004, China. Electronic address:

Posterior capsule opacification (PCO) is the most common complication after cataract surgery. In this study, we used transforming growth factor beta-2 (TGF-β2)-induced SRA01/04 cells to mimic PCO cell model and explored the functions and underlying mechanisms of specific protein 1 (SP1) in TGF-β2-induced SRA01/04 cell development. MTT assay and EdU assay were carried out to explore the proliferation of SRA01/04 cells.

View Article and Find Full Text PDF

Aim: To investigate the biocompatibility and bacterial adhesion properties of light responsive materials (LRM) and analyze the feasibility and biosafety of employing LRM in the preparation of accommodative intraocular lenses (AIOLs).

Methods: Employing fundamental experimental research techniques, LRM with human lens epithelial cells (hLECs) and human retinal pigment epithelium cells (ARPE-19 cells) were co-cultured. Commercially available intraocular lenses (IOLs) were used as controls to perform cell counting kit-8 (CCK-8), cell staining under varying light intensities, cell adhesion and bacterial adhesion experiments.

View Article and Find Full Text PDF

Purpose: To report the clinical outcomes achieved in refractory cases of neurotrophic keratopathy (NK) through the utilization of insulin eye drops alone or in conjunction with a drug-depository contact lens (DDCL).

Observations: This multicentric prospective open-label uncontrolled case series included consecutive patients with NK refractory to conventional treatment. Insulin eye drops (1 unit/mL) were prescribed 4 times/day in all cases, and a Therapeutic Hyper-CL™ soft contact lens (EyeYon Medical, Ness Ziona, Israel), designed to act as a drug reservoir, was applied in selected patients.

View Article and Find Full Text PDF

Reprogramming of iPSCs to NPCEC-like cells by biomimetic scaffolds for zonular fiber reconstruction.

Bioact Mater

March 2025

Eye Institute and Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China.

Ectopia lentis (EL), characterised by impaired zonular fibers originating from non-pigmented ciliary epithelial cells (NPCEC), presents formidable surgical complexities and potential risks of visual impairment. Cataract surgery is the only treatment method for EL, but it leads to the loss of accommodative power of the lens post-operatively. Furthermore, the challenge of repairing zonular ligaments remains a significant global issue.

View Article and Find Full Text PDF

Phacoemulsification combined with intraocular lens implantation is the primary treatment for cataract. Although this treatment strategy benefits patients with cataracts, posterior capsule opacification (PCO) remains a common complication that impairs vision and affects treatment outcomes. The pathogenesis of PCO is associated with the proliferation, migration, and fibrogenesis activity of residual lens epithelial cells, with epithelial-mesenchymal transition (EMT) serving as a key mechanism underlying the condition.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!