MiR-30a inhibits BECN1-mediated autophagy in diabetic cataract.

Lu Zhang,Yusen Huang,Rong Cheng

doi:10.18632/oncotarget.20483

Lu Zhang, Yusen Huang + Show 1 more

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https://doi.org/10.18632/oncotarget.20483

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Abstract

PurposeTo investigate the role of microRNAs in the regulation of autophagy and apoptosis in lens epithelial cells (LECs) during diabetic cataract formation.MethodsA miRNA microarray study and quantitative real-time PCR were performed to identify the expression of miRNAs in LECs of diabetic cataract. Human LECs were cultured in high glucose conditions as a diabetic cataract model. BECN1 and LC3B were detected by Western blotting and quantitative real-time PCR. The extent of apoptosis was measured using FACSCalibur flow cytometry.ResultsDownregulation of miR-30a was identified in LECs attached to diabetic cataract tissues. By the bioinformatic assay and the luciferase activity assay, BECN1 was found to be a direct target of miR-30a. MiR-30a reduced the BECN1-mediated autophagy activity induced by high glucose in LECs in vitro. The ratio of LECs apoptosis was also decreased.ConclusionMiR-30a was involved in the inhibition of autophagy by targeting BECN1 in LECs in human diabetic cataract.

Highlights

Cataracts are a leading cause of blindness and visual impairment in the world [1]
Downregulation of miR-30a was identified in lens epithelial cells (LECs) attached to diabetic cataract tissues
MiR-30a reduced the BECN1-mediated autophagy activity induced by high glucose in LECs in vitro

Summary

Introduction

Cataracts are a leading cause of blindness and visual impairment in the world [1]. A significant relationship has been revealed between diabetes mellitus (DM) and diabetic cataract as the younger ages and severity of cataracts were found in diabetic patients [2]. One of the reasons may be the high glucose (HG) in such patients. Human lens epithelial cells (LECs) are a single layer of polygonal cuboidal cells that act as the major source of transport, metabolism and detoxification in lens development [3]. The integrity and survival of LECs are critical for lens transparency [4]. The molecular mechanism during the process of diabetic cataract formation remains largely unknown

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