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。 |
关键词: 长链非编码RNA-linc00152 血管内皮细胞 细胞凋亡 细胞迁移 miR-4767 |
DOI: |
分类号:R 394.2; R 45 |
基金项目:河南省高等学校重点科研项目(18A320023). |
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Long-chain non-coding RNA-linc00152 expression may play a role in apoptosis and migration of vascular endothelial cells via miR-4767 |
TENG Wei, ZHENG Xian-jie*, GONG Gui-hong, HE Zhao-hui, ZHANG Jun-yi, HUI Xue-zhi
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Department of Cardiology, the First Affiliated Hospital of Henan University, Kaifeng 475001, Henan, China
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Abstract: |
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 Bc12L12 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. |
Key words: lncRNA-linc00152 vascular endothelial cells apoptosis migration miR-4767 |