首页|雷帕霉素上调人脐静脉内皮细胞自噬活性抑制细胞增殖

雷帕霉素上调人脐静脉内皮细胞自噬活性抑制细胞增殖

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目的 探讨人脐静脉内皮细胞(HUVECs)自噬激活对细胞增殖的影响.方法 使用雷帕霉素(Rapa)处理HU-VECs,Western blot法检测微管相关蛋白1 轻链3(LC3)、Be-clin 1 和unc-51 样激酶1(ULK1)的表达,透射电镜(TEM)检测自噬小体,丹酰尸胺染色(MDC)检测自噬荧光;CCK-8 法和EdU法检测自噬激活对细胞增殖的影响;血管形成实验检测成管能力.结果 Rapa 处理后,与对照组相比,LC3、Beclin 1 和ULK1 表达增强,实验组绿色自噬荧光表达强于对照组,TEM可见自噬小体;CCK-8 和EdU结果显示,与对照组相比,实验组细胞自噬活化后细胞增殖能力减弱,成管能力降低.结论 在一定时间内,Rapa上调HUVECs自噬活性抑制细胞增殖.
Rapamycin upregulates autophagy inhibits cell proliferation in human umbilical vein endothelial cells
Objective To investigate the effect of autophagy activation on cell proliferation in human umbilical vein endothelial cells(HUVECs).Methods HUVECs were treated with rapamycin(Rapa).Western blot assay was performed to examine the expression of protein of microtubule associated protein 1 light chain 3(LC3),Beclin 1 and unc-51-like kinase 1(ULK1).Autophagosomes were detected by transmission electron microscopy(TEM),and autophagy fluorescence was detected by monodansylcadaverine staining(MDC)assay.The effect of autophagy activation on cell proliferation was assessed by CCK-8 assay and EdU assay.Vascular formation experiments were used to detect vasculogenic ability.Results After Rapa treatment,LC3,Beclin1 and ULK1 expressions were en-hanced,while the green autophagy fluorescence expression in the experimental group was stronger than that in the control group,and autophagosomes were visible by TEM;CCK-8 and EdU results showed that compared with the control group,the cell proliferation ability was weakened and tubes formation ability was reduced after the activation of autophagy in experimental cells.Conclusion Rapa upregulates autophagy activity in HUVECs to inhibit cell proliferation under certain time.

rapamycinHUVECsautophagyautophagic activityautophagic proteincell proliferation

王雅雯、程亚楠、杨宾、苏碧昊、徐普

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中南大学湘雅医学院附属海口医院口腔中心·海南省口腔医学中心口腔综合科,海口 570208

雷帕霉素 人脐静脉内皮细胞 自噬 自噬活性 自噬蛋白 细胞增殖

国家自然科学基金海南省重点研发计划海南省自然科学基金高层次人才项目海南省自然科学基金高层次人才项目

82060194ZDYF2022SHFZ119821RC727821RC725

2024

安徽医科大学学报
安徽医科大学

安徽医科大学学报

CSTPCD北大核心
影响因子:1.095
ISSN:1000-1492
年,卷(期):2024.59(4)
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