SP1-mediated lncRNA PVT1 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract via miR-214-3p/MMP2 axis.

Jun Yang,Shaozhen Zhao,Fang Tian

doi:10.1111/jcmm.14762

Jun Yang, Shaozhen Zhao + Show 1 more

Open Access

https://doi.org/10.1111/jcmm.14762

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Abstract

Emerging evidence illustrates the critical roles of long non‐coding RNAs (lncRNAs) in the diabetes. However, the deepgoing regulation of lncRNA PVT1 in the diabetic cataract (DC) is still unclear. Here, present research investigates the pathologic roles and underlying mechanism by which lncRNA PVT1 regulates the DC pathogenesis. Human lens epithelial (HLE) B‐3 cells were induced by the high glucose (HG) to simulate the DC microenvironment models. Results revealed that lncRNA PVT1 expression was up‐regulated in the HG‐induced HLE B‐3 cells as compared to the normal glucose group. Transcription factor SP1 could bind with the promoter region of PVT1 and activate its transcription. Functionally, PVT1 knock‐down could repress the proliferation and promote the apoptosis of HLE B‐3 cells. Mechanistically, PVT1 acted as the ‘miRNA sponge’ to target miR‐214‐3p/MMP2 axis. This finding revealed a novel insight of lncRNA PVT1 for the DC pathogenesis, providing an inspiration for the DC mechanism.

Highlights

Diabetes mellitus could arouse a series of complications, including abnormal blood distribution, microcirculation abnormity and metabolic disorders.[1,2] For the eyes, the terminal circulation anomaly could trigger the cataract
LncRNA PVT1 has been reported as a diabetes-related non-coding RNAs (ncRNAs) transcript.[19,20,21]
We found that the Long non-coding RNAs (lncRNAs) PVT1 was remarkedly up-regulated in the diabetic cataract (DC) tissue and high glucose (HG)-administrated Human lens epithelial (HLE) B-3 cells

Summary

| INTRODUCTION

Diabetes mellitus could arouse a series of complications, including abnormal blood distribution, microcirculation abnormity and metabolic disorders.[1,2] For the eyes, the terminal circulation anomaly could trigger the cataract. The high glucose (HG) could cause the lens metabolism disorder, thereby inducing the diabetic cataract (DC).[3,4] Human lens epithelial cells (HLECs) suffer the apoptosis and injure from HG environment in the pathogenesis of DC.[5,6]. | 555 neurons impairment by synaptic plasticity and apoptosis in diabetes.[13] Transcription factor specificity protein 1 (Sp1) is found to participate in the oxidative stress-driven aberrant Sumoylation signalling of lens epithelial cells.[14] In the present research, we found that lncRNA PVT1 was significantly up-regulated in the diabetic cataract tissue and the high glucose-induced lens epithelial cell line (HLE B3). SP1-mediated lncRNA PVT1 overexpression modulated the proliferation and apoptosis of HLE B3 cells via miR-214-3p/MMP2 axis. This finding revealed a novel insight of lncRNA PVT1 for the DC pathogenesis, providing an inspiration for the DC mechanism

| MATERIALS AND METHODS

Findings

| DISCUSSION