FoxO1和FoxO3a在内皮细胞凋亡过程中的作用  

The roles of FoxO1 and FoxO3a in endothelial cell apoptosis

作　　者：曲环[1] 李芳[2] 

机构地区：[1]北京大学深圳医院心内科,广东深圳518000 [2]深圳北京大学香港科技大学医学中心生物医学研究所,广东深圳518000

出　　处：《广东医学》2016年第21期3162-3164,共3页Guangdong Medical Journal

基　　金：深圳科学技术项目(编号:201103019;KQCX20120803145850990)

摘　　要：目的探索肝细胞生长因子(HGF)在内皮细胞中是否通过磷酸化FoxO1及FoxO3a的机制发挥其抗凋亡活性。方法分离与原代培养人脐静脉内皮细胞(HUVEC),由100μmol H_2O_2诱导损伤,分空白对照组、100μmol H_2O_2组和HGF预处理30 min后加100μmol H_2O_2组,通过流式细胞仪判定细胞凋亡程度及Western blot检测蛋白含量变化。结果 H_2O_2处理对数生长期的HUVEC 24 h会导致(82.74±1.53)%的细胞凋亡,HGF预处理细胞后,细胞凋亡比例降至(25.4±3.69)%,两组相比差异有统计学意义(P<0.05);HGF可时间依赖性地磷酸化FoxO1及FoxO3a。结论 HGF通过提高细胞内FoxO1和FoxO3a磷酸化水平,抑制H_2O_2所引起的HUVEC的凋亡。Objective To explore whether FoxO1 and FoxO3a mediated the anti - apoptosis mechanism of hepa- tocyte growth factor （HGF） in mature endothelial cells through phosphorylation. Methods Endothelial cells were separa- ted from neonatal umbilical vein. The primary cultured cells were divided into control group, H2O2 group and HGF- H2O2 group. Flow Cytometry （FCM） was used to analyze cell apoptosis induced by 100 μM H2O2 and Western Blot were carried out to evaluated the related protein expression. Results HGF up - regulated the phosphorylation level of FoxO1 and FoxO3a, and reduced the H2O2 - induced apoptosis of HUVEC. Conclusion HGF could inhibit HUVEC apoptosis induced by H2O2, probably via FoxO proteins phosphorylation.

关 键 词：FOXO1 FOXO3A 肝细胞生长因子 内皮细胞 

分 类 号：R543.5[医药卫生—心血管疾病]