摘要
目的:探讨长链非编码RNA(lncRNA)-linc00152在静脉血管内皮细胞(vascular endothelial cells, VECs)凋亡和迁移中的作用及其机制。方法:用溶于磷酸盐缓冲液(PBS)的氧化低密度脂蛋白(ox-LDL)处理人脐静脉血管内皮细胞(human umbilical vein endothelial cell, HUVEC)。通过载体转染、蛋白质印迹、荧光素酶构建、生物素化等检测HUVEC中linc00152与miR-4767的相互作用,以及两者对HUVEC凋亡、迁移的影响及相关机制。结果:linc00152负向调节HUVEC中miR-4767的表达(P<0.05)。miR-4767促进HUVEC的凋亡,抑制HUVEC的迁移;linc00152抑制HUVEC的凋亡,促进HUVEC的迁移(P<0.05)。阻断miR-4767后,linc00152敲减引起的HUVEC凋亡增加与迁移减少的作用被减弱;同时,linc00152敲减引起的Bcl2L12和表皮生长因子受体(epidermal growth factor receptor, EGFR)蛋白表达的减少被改善。结论:linc00152可能成为改善血管内皮功能和治疗部分心血管疾病的潜在靶点。
Objective:To explore the role of long-chain non-coding RNA(lncRNA)-linc00152 in the apoptosis and migration of vascular endothelial cells(VECs)and the underlying mechanisms.Methods:Human umbilical vein endothelial cell(HUVEC)were treated with oxidized-low density lipoprotein(ox-LDL)which was solving in fetal bovine serum(FBS).The interactions of linc00152 and miR-4767 in HUVEC were detected by transfection of vectors,Western blotting,luciferase construction,and biotinylation analysis.Then the effects of miR-4767 and linc00152 on the apoptosis and migration of HUVEC and the underlying mechanisms were explored.Results:The expression of miR-4767 was negatively regulated by linc00152(P<0.05).miR-4767 increased the apoptosis of HUVEC and decreased their migration;linc00152 decreased the apoptosis of HUVEC and increased their migration(P<0.05).After blocking miR-4767,the apoptosis and migration induced by linc00152 knockdown were reduced,meanwhile,the decrease of Bc12 L12 and epidermal growth factor receptor(EGFR)induced by linc00152 knockdown were attenuated.Conclusions:Linc00152 may become a potential therapeutic target for improving vascular endothelial function and treating some cardiovascular diseases.
作者
滕伟
郑先杰
巩贵宏
何兆辉
张君毅
惠学志
TENG Wei;ZHENG Xian-jie;GONG Gui-hong;HE Zhao-hui;ZHANG Jun-yi;HUI Xue-zhi(Department of Cardiology,the First Affiliated Hospital of Henan University,Kaifeng 475001,Henan,China)
出处
《中国临床医学》
2019年第2期209-214,共6页
Chinese Journal of Clinical Medicine
基金
河南省高等学校重点科研项目(18A320023)~~
