武汉大学人民医院健康管理中心 湖北 武汉 430060
李颖,女,1982—,医学博士,主要从事糖尿病视网膜病变分子机制研究,E⁃mail: 36252080@qq.com
徐丽娟,女,1979—,医学硕士,副主任医师,主要从事慢病健康管理及分子机制研究,E⁃mail: zoe0512@163.com
收稿:2025-01-11,
纸质出版:2025-11-25
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李颖,何璐,林任等.长链非编码RNA PVT1通过miR⁃20a⁃5p/VEGFA轴调控糖尿病视网膜病变视网膜色素上皮细胞[J].武汉大学学报(医学版),2025,46(11):1399-1405.
LI Ying,HE Lu,LIN Ren,et al.Long non⁃coding RNA PVT1 regulates retinal pigment epithelial cells in diabetic retinopathy via the miR⁃20a⁃5p/VEGFA axis[J].Medical Journal of Wuhan University,2025,46(11):1399-1405.
李颖,何璐,林任等.长链非编码RNA PVT1通过miR⁃20a⁃5p/VEGFA轴调控糖尿病视网膜病变视网膜色素上皮细胞[J].武汉大学学报(医学版),2025,46(11):1399-1405. DOI: 10.14188/j.1671-8852.2025.0044.
LI Ying,HE Lu,LIN Ren,et al.Long non⁃coding RNA PVT1 regulates retinal pigment epithelial cells in diabetic retinopathy via the miR⁃20a⁃5p/VEGFA axis[J].Medical Journal of Wuhan University,2025,46(11):1399-1405. DOI: 10.14188/j.1671-8852.2025.0044.
目的
2
探讨长链非编码RNA(lnc RNA)浆细胞瘤变异易位基因1(PVT1)通过结合miR⁃20a⁃5p调控血管内皮生长因子A(VEGFA)表达在糖尿病视网膜病变(DR)视网膜色素上皮细胞(RPEs)中的作用及其分子机制。
方法
2
借助生物信息学工具预测DR中的分子机制。采用qRT⁃PCR检测玻璃体和RPEs中PVT1、miR⁃20a⁃5p和VEGFA的表达。CCK⁃8和流式细胞术观察PVT1/miR⁃20a⁃5p/VEGFA对RPEs增殖和凋亡的影响。双荧光素酶报告基因实验验证PVT1和miR⁃20a⁃5p、miR⁃20a⁃5p和VEGFA的相互作用关系。
结果
2
PVT1和VEGFA在DR患者的玻璃体和高糖损伤模型组RPEs中高表达。敲低PVT1能显著促进高糖损伤RPEs增殖,抑制RPEs凋亡。miR⁃20a⁃5p抑制剂或过表达VEGFA均可部分逆转敲低PVT1对高糖损伤RPEs增殖和凋亡的调控作用,RPEs中存在PVT1/miR⁃20a⁃5p/VEGFA互作网络。
结论
2
敲低PVT1可通过PVT1/miR⁃20a⁃5p/VEGFA轴对高糖损伤的RPEs起到保护作用。
Objective
2
To investigate the role and underlying molecular mechanisms by which the long non⁃coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) regulates vascular endothelial growth factor A (VEGFA) expression in retinal pigment epithelial cells (RPEs) via its interaction with miR⁃20a⁃5p in diabetic retinopathy (DR)
Methods
2
Bioinformatics tools were used to predict the molecular mechanisms in DR. The expression levels of PVT1
miR⁃20a⁃5p
and VEGFA in vitreous humor and RPEs were detected by qRT⁃PCR. The effects of the PVT1/miR⁃20a⁃5p/VEGFA axis on the proliferation and apoptosis of RPEs were assessed using the CCK⁃8 assay and flow cytometry. The interaction between PVT1 and miR⁃20a⁃5p
as well as between miR⁃20a⁃5p and VEGFA
were verified by dual⁃luciferase reporter assays.
Results
2
PVT1 and VEGFA were highly expressed in the vitreous of DR patients and in RPEs in the high⁃glucose injury model group. Knockdown of PVT1 significantly promoted proliferation and inhibited apoptosis in high⁃glucose⁃injured RPEs. Both miR⁃20a⁃5p inhibitors and overexpression of VEGFA could partially reverse the regulatory effects of PVT1 knockdown on the proliferation and apoptosis of high⁃glucose⁃injured RPEs
suggesting the existence of a PVT1/miR⁃20a⁃5p/VEGFA interaction network in RPEs.
Conclusion
2
Knockdown of PVT1 can protect high⁃glucose injured RPEs via the PVT1/miR⁃20a⁃5p/VEGFA axis.
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