Abstract

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.

Highlights

  • Cataract, an eye lens opacification, can lead to serious reversible visual impairment and blindness, and is a multifactorial disease caused by various factors, amongst which diabetes is an essential one [1,2]

  • We investigated the influence of miR-211 on the proliferation and apoptosis of lens epithelial cells in diabetic cataract mice by targetting the sirtulin 1 (SIRT1) gene

  • Our results mainly demonstrated that inhibiting the miR-211 expression could diminish the rate of apoptosis of lens epithelial cells in diabetic cataract mice whereas silencing the SIRT1 gene could stimulate the rate of apoptosis of lens epithelial cells in diabetic cataract mice

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Summary

Introduction

An eye lens opacification, can lead to serious reversible visual impairment and blindness, and is a multifactorial disease caused by various factors, amongst which diabetes is an essential one [1,2]. DM patients suffer from chronic complications with increasing morbidity and mortality; cataract and lens opacity are the earliest complications experienced by DM patients, which are characterized by severe metabolic disorders and high blood glucose level [5,6]. Clinical epidemiology and basic research have confirmed an association between diabetic retinopathy and cataract formation [4,7]. Lens epithelial cell apoptosis is a common cellular foundation for the development of non-congenital cataract in human beings and animals [8]. Former evidence revealed that high glucose concentrations could lead to apoptosis of human lens epithelial cell and inhibit proliferation [9]. MiRNA has been widely studied for its close association with lens epithelial cells [10-12]

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