Page 45 - 南京医科大学学报自然科学版

第43卷第2期 南京医科大学学报（自然科学版）
2023年2月 Journal of Nanjing Medical University（Natural Sciences） ·187 ·

·基础医学·

LncRNA VIM⁃AS1 通过 miR⁃497⁃5p/FBXW7 轴调控高糖环境下

视网膜内皮细胞的迁移和凋亡

居悦俊，郭展宏，王冠怡，沈 婷，吴润泽，孔颖宏 *

常熟市第二人民医院内分泌科，江苏 常熟 215500

［摘 要］ 目的：探讨长链非编码RNA（lncRNA）VIM反义RNA 1（VIM⁃AS1）在糖尿病视网膜病变中的潜在分子机制。方法：
使用qRT⁃PCR测定 LncRNA VIM⁃AS1、miR⁃497⁃5p和FBXW7 mRNA的表达。使用蛋白质印迹检测FBXW7蛋白水平。分别使
用CCK⁃8实验、伤口愈合实验和流式细胞技术分析评估细胞增殖、迁移和凋亡。通过双荧光素酶报告基因分析验证lncRNA
VIM⁃AS1、miR⁃497⁃5p和FBXW7之间的结合关系。结果：在高糖处理的ARPE⁃19细胞中，LncRNAVIM⁃AS1和 FBXW7的表达

显著降低，而miR⁃497⁃5p的表达上调。LncRNA VIM⁃AS1可以通过竞争性结合miR⁃497⁃5p上调FBXW7的表达。LncRNA VIM⁃
AS1过表达能够促进HG处理的ARPE⁃19细胞的增殖和迁移，并抑制细胞凋亡，而miR⁃497⁃5p过表达消除了lncRNA VIM⁃AS1
过表达对HG处理的ARPE⁃19细胞的影响。此外，FBXW7敲低消除了miR⁃497⁃5p 对HG处理的ARPE⁃19细胞表型的抑制。结
论：lncRNA VIM⁃AS1 可通过调控 miR⁃497⁃5p/FBXW7 轴促进 HG 处理的 ARPE⁃19 细胞增殖和迁移，同时抑制细胞凋亡，提示
lncRNA VIM⁃AS1作为治疗靶点潜力巨大。
［关键词］ LncRNA VIM⁃AS1；miR⁃497⁃5p；FBXW7；糖尿病视网膜病变；人视网膜上皮细胞
［中图分类号］ R774.1 ［文献标志码］ A ［文章编号］ 1007⁃4368（2023）02⁃187⁃10
doi：10.7655/NYDXBNS20230206

LncRNA VIM⁃AS1 regulates cell migration and apoptosis of retinal endothelialcells under
high glucose treatment via the miR⁃497⁃5p/FBXW7 axis
JU Yuejun，GUO Zhanhong，WANG Guanyi，SHEN Ting，WU Runze，KONG Yinghong *
Department of Endocrinology，Changshu No.2 People’s Hospital，Changshu 215500，China

［Abstract］ Objective：Our study aimed to probe the potential molecular mechanism of long non ⁃ coding RNA（lncRNA）VIM
Antisense RNA 1（VIM⁃AS1）in diabetic retinopathy. Methods：LncRNA VIM⁃AS1，miR⁃497⁃5p and FBXW7 mRNA expressions were
determined using qRT ⁃ PCR. The FBXW7 protein level was also detected using western blotting. The cell viability，migration and
apoptosis were evaluated using CCK⁃8 assay，wound healing assay and flow cytometry analysis，respectively. Additionally，the binding
relationships among lncRNA VIM⁃AS1，miR⁃497⁃5p and FBXW7 were verified by dual luciferase reporter assaies. Results：LncRNA
VIM⁃AS1 and FBXW7 expressions were remarkably reduced in HG⁃treated ARPE⁃ 19 cells，while miR⁃497⁃5p was upregulated.
LncRNA VIM ⁃ AS1 could upregulate the expression of FBXW7 by competitively binding to miR ⁃ 497 ⁃ 5p. LncRNA VIM ⁃ AS1
overexpression promoted cell proliferation and migration，and inhibited cell apoptosis in HG⁃induced ARPE⁃19 cells，while miR⁃497⁃
5p overexpression abolished the effects of lncRNA VIM⁃AS1 overexpression on HG⁃induced ARPE⁃19 cells. Furthermore，FBXW7
knockdown abrogated the effects of miR⁃497⁃5p inhibition on cell phenotypes of HG⁃treated ARPE⁃19 cells. Conclusion：LncRNA
VIM⁃AS1 could promote the proliferation and migration，while inhibited cell apoptosis of HG⁃treated ARPE⁃19 cells by regulation of
miR⁃497⁃5p/FBXW7 axis，suggesting that lncRNA VIM⁃AS1 might have great potential as therapeutic target for diabetic retinopathy.
［Key words］ LncRNA VIM⁃AS1；miR⁃497⁃5p；FBXW7；diabetic retinopathy；human retinal epithelial cells
［J Nanjing Med Univ，2023，43（02）：187⁃195，248］

［基金项目］ 常熟市卫生健康委员会科技计划指导项目（CSWZD202110）；常熟市第二人民医院面上项目（CSEY2021041）
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通信作者（Corresponding author），E⁃mail：kongyinghong@163.com