高糖干预骨髓来源MAPC细胞周期的研究  

Regulation of Cell Cycle of MAPCs via High-glucose

作　　者：罗旻[1] 刘泽灏[1] 李纯[1] 

机构地区：[1]中南大学湘雅医院内分泌科,中国湖南长沙410078

出　　处：《生命科学研究》2015年第3期229-236,共8页Life Science Research

基　　金：湖南省科学技术厅科技计划一般项目(2012fj4352)

摘　　要：骨髓来源MPAC是具有多向分化潜能的成体干细胞,高糖是干扰MAPC细胞分化趋势的重要因素。通过流式细胞技术分析高糖对MAPC细胞周期的影响。研究显示,高糖迟滞MAPC细胞的细胞周期在G1/S期。进一步研究的结果提示,高糖可以通过TGF-β1调控ERK1/2信号通路,选择性上调P21蛋白表达,抑制MAPC的细胞周期进程,此时的MAPC细胞Oct4高表达,具有多项分化能力(处于非分化状态)。Multipotent adult progenitor cells（MAPCs） derived from bone marrow stem cell,with multi-directional differentiation. High glucose is one of the important interferential factors for the differentiation of MAPCs. FACS was performed for analysis of cell cycle of MAPCs incubated in high-glucose（HG）. The data indicated that cell cycle of MAPCs was arrested in G1/S. The mechanism indicated that cell cycle of MAPCs was arrested via high glucose-induced expression of TGF-β1, with up-regulation expression of P21 via ERK1/2 signaling. At the same time, high-expression level of Oct4 in MAPCs exhibit extensive expansion capability and are able to differentiate at the single cell level into functional multiple cell lineages of all three germinal layers（un-differentiation）.

关 键 词：高糖 MAPC细胞 细胞周期 TGF-Β1 P21 ERK1/2 

分 类 号：R587.1[医药卫生—内分泌]