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作 者:潘意 毛宇飞[1] 余勇[1] 王文倩 陈浩浩[1] PAN Yi;MAO Yufei;YU Yong;WANG Wenqian;CHEN Haohao(Medical Molecular Biology Laboratory,School of Medicine,Jinhua Polytechnic,Jinhua,Zhejiang 321007,China)
机构地区:[1]金华职业技术学院医学院分子生物学实验室,浙江金华321007
出 处:《医药前沿》2023年第8期17-21,共5页Journal of Frontiers of Medicine
基 金:金华市科学技术研究计划项目(2020-4-091,2021-3-149);浙江省教育厅访问工程师校企合作项目(FG2019029)。
摘 要:目的:探讨多肽C16能否有效通过Ang1/Tie2-PI3K/AKT通路促进人脐静脉内皮细胞(HUVEC)的迁移及血管化。方法:体外培养HUVEC,实验分为Control组、Tie2激酶抑制剂组(Tie2 KI组)、Tie2激酶抑制剂+C16/COMP-Ang1组(Tie2 KI+C16/COMP-Ang1组)。通过实时无标记细胞分析检测C16/COMP-Ang1对细胞增殖的影响,划痕试验和小管形成检测HUVEC迁移和血管化能力,鬼笔环肽检测细胞骨架重排能力,Western blot检测Tie2及AKT的磷酸化水平,探讨多肽C16/COMP-Ang1是否通过Ang1/Tie2-PI3K/AKT通路来促进HUVEC的迁移及血管化。结果:C16/COMP-Ang1提高HUVEC的Tie2及AKT的磷酸化水平,与单用Tie2抑制剂组比较,使用C16/COMP-Ang1后,细胞的迁移能力提高,“管道样”结构形成增多,细胞内微丝束数量增加,细胞增殖能力也明显上升。结论:C16/COMP-Ang1能通过Ang1/Tie2-PI3K/AKT通路促进HUVEC的迁移及血管化。Objective To investigate whether peptide C16 can effectively promote the migration and vascularization of HUVEC through the Ang1/Tie2-PI3K/AKT pathway.Methods HUVEC was cultured in vitro and divided into Control group,Tie2 kinase inhibitor group(Tie2 KI group),and Tie2 kinase inhibitor+C16/COMP-Ang1 group(Tie2 KI+C16/COMP-Ang1 group).The effects of C16/COMP-Ang1 on cell proliferation were detected by real-time unlabeled cell analysis,HUVEC migration and vascularization were detected by scratch test and tubule formation,cytoskeleton rearrangement was detected by phalloidin,and phosphorylation levels of Tie2 and AKT were detected by Western blot to explore whether the polypeptide C16/COMP-Ang1 could promote HUVEC migration and vascularization through Ang1/Tie2-PI3K/AKT pathway.Results C16/COMP-Ang1 increased the phosphorylation levels of Tie2 and AKT in HUVEC.Compared with the Tie2 inhibitor group alone,the use of C16/COMP-Ang1 improved the migration ability of cells,increased the formation of“pipeline like”structures,increased the number of intracellular microfilaments,and significantly increased cell proliferation ability.Conclusion C16/COMP-Ang1 can promote the migration and vascularization of HUVEC through the Ang1/Tie2-PI3K/AKT pathway.
关 键 词:多肽C16 血管内皮细胞 血管化 PI3K/AKT
分 类 号:R543[医药卫生—心血管疾病]
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