磷酸肌醇3激酶／蛋白激酶B信号通路在基质细胞衍生因子-1诱导的Tip血管内皮细胞迁移中的作用  

The role of phosphatidylinositol 3 kinase/protein kinase B in stromal cell derived factor -1 induced migration of endothelial Tip cell

作　　者：杜玲娟[1] 杨镛[1] 杨国凯[1] 马振桓[1] 李国剑[1] 万嘉[1] Du Lingjuan;Yang Yong;Yang Guokai;Ma Zhenhuan;Li Guojian;Wan Jia(Department of Vascular Surgery, the Fourth Hospital Affiliated Kunming Medical College, the Second People＇ s Hospital of Yunnan Province, Yunnan Province Vascular Surgery Center, the First Hospital of Yunnan University, Abdominal Minimally Invasive Surgery Research Center of Yunnan Province, Kunming 650021, China)

机构地区：[1]昆明医科大学第四附属医院血管外科云南省第二人民医院云南省血管外科中心云南大学第一医院云南省腹部微创外科研究中心,650021

出　　处：《中华实验外科杂志》2018年第7期1199-1202,共4页Chinese Journal of Experimental Surgery

基　　金：云南省应用基础研究计划-昆医联合专项（2014FZ041）;云南省卫生内设研究课题（2016NS188、2017NS137）

摘　　要：目的磷酸肌醇3激酶（P13K）／蛋白激酶B（Akt）信号通路在基质细胞衍生因子-1（SDF-1）诱导的Tip内皮细胞迁移中的作用。方法采用密度梯度离心法从人外周血单个核细胞中分离培养出血管内皮祖细胞，并将其诱导分化为Tip内皮细胞，将TiP内皮细胞随机分成阴性对照组、AMD3100对照组、LY294002对照组、实验组、AMD3100阻断组、LY294002阻断组、外源性PIP3组，Transwell迁移实验检测各组中Tip内皮细胞的迁移数。结果实验组迁移到下室的细胞数量[（100．667±4．509）个／高倍视野]较阴性对照组[（16．333±2．082）个／高倍视野]增多（t=29．415，P=0．003），AMD3100阻断剂组迁移到下室的细胞数[（20．333±0．577）个／高倍视野]与阴性对照组比较，差异无统计学意义（t=2．590，P=0．096），AMD3100阻断剂组和LY294002阻断剂组迁移到下室的细胞数分别为（20．333±0．577）、（40．000±2．646）个／高倍视野，均小于实验组（t=30．603、20．102．P=0．019、0．006），而在AMD3100阻断剂组中外源性的加人磷脂酰肌醇3激酶（P13K）产物PIP3，迁移到下室的细胞数[（99．667±3．786）个／高倍视野]与实验组比较差异无统计学意义（t=0．294，P=1．000）。结论P13K／Akt信号通路是SDF-1诱导Tip血管内皮细胞迁移的下游机制之一。Objective To investigate the effect of phosphatidy]inositol 3 kinase （ PI3K）/protein kinase B （Akt） in Endothelial Tip Cell migration induced by stromal cell derived factor - 1 （ SDF - 1 ）. Methods The cultured peripheral blood mononuclear cells in vitro were acquried by density gradient - centrifilgation, andthe endothelial progenitor cells were isolated and cultivated form the peripheralblood mononuclear cells, the endothelial progenitor cells were differentiated into Tip vascular endothelial ceils. Then, the Tip ceils were divided into negative control group, AMD3100 control group, LY294002 control group, experimental group, AMD3100 blocked group, LY294002 blocked group and exogenous PIP3 added group, the abilities of migration of Tip vascular endothelial ceils in different groups were measured by the methods of transwell migration experiment. Results More ceils migrated to lower chamber in experimental group （ 100. 667 ± 4. 509 ） compared with negative control group （ 16. 333 ± 2. 082） （ t = 29. 415, P = 0. 003）, the migration of the Tip endothelial Cells were not significant between AMD3100 blocked group （20. 333 ± 0. 577） and negative control group （ t = 2. 590, P = 0. 096）. less cells migrated to lower chamber in AMD3100 blocked group （20. 333 ±0. 577 ）and PI3K blocked group （40. 000± 2. 646 ） compared with experimental group （t = 30. 603, 20. 102, P = 0. 019, 0. 006）. However, there was no difference between exogenous PIP3 added group （99. 667 ±3. 786） and experimental group （ t = 0. 294, P = 1. 000 ）. Conclusion PI3K/Akt Pathway is the downstream mechanism of migration of endothelial Tip cells induced by SDF- 1.

关 键 词：磷酸肌醇3激酶/蛋白激酶B 基质细胞衍生因子-1 Tip内皮细胞 细胞迁移 

分 类 号：R329.2[医药卫生—人体解剖和组织胚胎学]