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

MiR-30a inhibits BECN1-mediated autophagy in diabetic cataract.
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MiR-30a 抑制糖尿病白内障中 BECN1 介导的自噬

DOI:
10.18632/oncotarget.20483
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发表时间:
2017-09-29
期刊:
影响因子:
--
通讯作者:
Huang Y
Huang Y
中科院分区:
其他
文献类型:
--
作者:
Zhang L;Cheng R;Huang Y

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目的探讨microrna在糖尿病性白内障形成过程中对晶状体上皮细胞(LECs)自噬和凋亡的调控作用。方法采用miRNA微阵列技术和实时荧光定量PCR技术检测糖尿病性白内障lec中miRNA的表达。在高糖条件下培养人LECs作为糖尿病性白内障模型。采用Western blotting和实时荧光定量PCR检测BECN1和LC3B。流式细胞术检测细胞凋亡程度。结果在糖尿病性白内障组织附着的LECs中发现miR-30a下调。通过生物信息学实验和荧光素酶活性实验发现BECN1是miR-30a的直接靶点。MiR-30a在体外降低becn1介导的高糖诱导的LECs自噬活性。细胞凋亡比例明显降低。结论MiR-30a通过靶向BECN1参与糖尿病性白内障LECs自噬的抑制。
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 in vitro. 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.
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