Rapamycin and 3-methyladenine regulate apoptosis and autophagy in bone-derived endothelial progenitor cells

作     者：LEI Feng-rui LI Xiao-qiang LIU Hui ZttU Ren-da MENG Qing-you RONG Jian-jie 

作者机构：Soochow Univ Dept Vasc Surg Affiliated Hosp 2 Suzhou 215004 Jiangsu Peoples R China First Peoples Hosp Wuxi Dept Gengral Surg Wuxi 214002 Jiangsu Peoples R China Peoples Hosp Haining Dept Gengral Surg Haining 314400 Zhejiang Peoples R China 

出 版 物：《Chinese Medical Journal》 (中华医学杂志（英文版）)

年 卷 期：2012年第125卷第22期

页      面：4076-4082页

核心收录：

学科分类：0710[理学-生物学] 1007[医学-药学(可授医学、理学学位)] 100705[医学-微生物与生化药学] 1002[医学-临床医学] 07[理学] 071003[理学-生理学] 10[医学] 

基　　金：The work was supported by a grant from the National Natural Science Foundation of China 

主　　题：apoptosis autophagy endothelialprogenitor cells rapamycin 3-methyladenine 

摘      要：Background Mammalian target of rapamycin （mTOR） is involved in a caspase independent form of programmed cell death called autophagy. The aim of this research was to investigate the effects of rapamycin and 3-methyladenine （3-MA） on autophagy, proliferation, apoptosis, and cell-cycle parameters of rat bone marrow-derived endothelial progenitor cells （EPCs）. Methods Mononuclear cells isolated from rat bone marrow were treated with rapamycin （0.01, 0.1, 1, or 10 pg/L） or 3-MA （1.25, 2.5, 5, or 10 mmol/L） for 24 hours. Expression of the autophagy marker protein LC3-11 was analyzed by Western blotting. Apoptosis and cell-cycle progression were analyzed by flow cytometry. Cell proliferation was measured using the MTT assay. Results Rapamycin treatment of EPCs induced apoptosis and autophagy and inhibited proliferation and cell-cycle progression in a dose-dependent manner. Treatment with 5 mmol/L 3-MA promoted cell proliferation; in contrast, treatment with 10 mmol/L 3-MA promoted apoptosis and induced S-phase arrest. Conclusions Rapamycin treatment of EPCs induced apoptosis and autophagy. Low concentrations of 3-MA had no significant effect on the proliferation and apoptosis of EPCs; The 5 mmol/L group promoted cell proliferation, but had no effect on the apoptosis; the 10 mmol/L group inhibited the proliferation and promoted apoptosis through the cell cycle.