PGC-1α prevents apoptosis in adipose-derived stem cells by reducing reactive oxygen species production in a diabetic microenvironment

被引:17
作者
Jiang, Xiao-Yan [1 ]
Lu, De-Bin [1 ]
Jiang, You-Zhao [1 ]
Zhou, Li-Na [1 ]
Cheng, Li-Qing [1 ]
Chen, Bing [1 ]
机构
[1] Third Mil Med Univ, Dept Endocrinol, Southwest Hosp, Chongqing 400038, Peoples R China
基金
中国国家自然科学基金;
关键词
Adipose-derived stem cells; Peroxisome proliferator activated receptor-gamma coactivator-1 alpha; Apoptosis; Mitochondria; Diabetes; OXIDATIVE STRESS; MITOCHONDRIAL BIOGENESIS; ENDOTHELIAL-CELLS; ANGIOGENESIS; DIFFERENTIATION; COMPLICATIONS; HYPERGLYCEMIA; DYSFUNCTION; MECHANISMS; PATHWAYS;
D O I
10.1016/j.diabres.2013.03.036
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Aims: To examine whether overexpression of peroxisome proliferator activated receptor-gamma coactivator-1 alpha (PGC-1 alpha) can prevent apoptosis in adipose-derived stem cells (ASCs) by reducing reactive oxygen species (ROS) production and enhancing mitochondrial function in a diabetic environment. Methods: After the isolation, expansion and characterisation of rat ASCs, we overexpressed PGC-1 alpha in ASCs using an adenoviral vector encoding green fluorescent protein (GFP) or PGC-1 alpha and tested the apoptotic effect under conditions of high glucose, hypoxia and serum deprivation. The production of intracellular ROS and mitochondrial ROS was evaluated using dihydroethidium and CM-H(2)XRos fluorescent probes. Results: Under conditions of high glucose, hypoxia and serum deprivation, the overexpression of PGC-1 alpha in ASCs decreased apoptosis and led to an increased survival rate. The ASCs modified with PGC-1 alpha produced lower intracellular and mitochondrial ROS. The mitochondrial morphology and structure in the PGC-1 alpha-ASC group remained relatively complete compared with the control group. Conclusions: These results reveal a crucial protective role for PGC-1 alpha in the treatment of diabetes mellitus and its complications using stem cells therapy. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:368 / 375
页数:8
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