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微小RNA-30a抑制糖尿病性白内障中BECN1介导的自噬。

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

作者信息

Zhang Lu, Cheng Rong, Huang Yusen

机构信息

Department of Ophthalmology, School of Medicine, Shandong University, Jinan 250012, China.

Qingdao Eye Hospital, Shandong Eye Institute, Shandong Academy of Medical Sciences, Qingdao 266071, China.

出版信息

Oncotarget. 2017 Aug 24;8(44):77360-77368. doi: 10.18632/oncotarget.20483. eCollection 2017 Sep 29.

DOI:10.18632/oncotarget.20483
PMID:29100392
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5652784/
Abstract

PURPOSE

To investigate the role of microRNAs in the regulation of autophagy and apoptosis in lens epithelial cells (LECs) during diabetic cataract formation.

METHODS

A 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.

RESULTS

Downregulation 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 . The ratio of LECs apoptosis was also decreased.

CONCLUSION

MiR-30a was involved in the inhibition of autophagy by targeting BECN1 in LECs in human diabetic cataract.

摘要

目的

研究微小RNA在糖尿病性白内障形成过程中对晶状体上皮细胞（LECs）自噬和凋亡调控中的作用。

方法

进行微小RNA微阵列研究和定量实时聚合酶链反应，以鉴定糖尿病性白内障LECs中微小RNA的表达。将人LECs在高糖条件下培养作为糖尿病性白内障模型。通过蛋白质免疫印迹法和定量实时聚合酶链反应检测自噬相关蛋白Beclin1（BECN1）和微管相关蛋白1轻链3β（LC3B）。使用FACSCalibur流式细胞仪测量细胞凋亡程度。

结果

在附着于糖尿病性白内障组织的LECs中发现miR-30a表达下调。通过生物信息学分析和荧光素酶活性测定，发现BECN1是miR-30a的直接靶点。miR-30a降低了高糖诱导的LECs中BECN1介导的自噬活性，同时LECs凋亡率也降低。

结论

在人类糖尿病性白内障的LECs中，miR-30a通过靶向BECN1参与自噬抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4965/5652784/b2b1c228506d/oncotarget-08-77360-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4965/5652784/b4409b47f86f/oncotarget-08-77360-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4965/5652784/33d2547f7f00/oncotarget-08-77360-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4965/5652784/cc04df9c0cd3/oncotarget-08-77360-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4965/5652784/b2b1c228506d/oncotarget-08-77360-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4965/5652784/b4409b47f86f/oncotarget-08-77360-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4965/5652784/33d2547f7f00/oncotarget-08-77360-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4965/5652784/cc04df9c0cd3/oncotarget-08-77360-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4965/5652784/b2b1c228506d/oncotarget-08-77360-g004.jpg

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