Nitric oxide-mediated immunosuppressive effect of human amniotic membrane-derived mesenchymal stem cells on the viability and migration of microglia

被引:17
作者
Yan, Ke [1 ,2 ]
Zhang, Run [1 ]
Chen, Lei [1 ]
Chen, Fanfan [1 ]
Liu, Yi [1 ]
Peng, Lingmei [1 ]
Sun, Haitao [1 ]
Huang, Weiyi [1 ]
Sun, Chengmei [1 ]
Lv, Bingke [1 ]
Li, Feng [1 ]
Cai, Yingqian [1 ]
Tang, Yanping [1 ]
Zou, Yuxi [1 ]
Du, Mouxuan [1 ]
Qin, Lingsha [1 ]
Zhang, Hengzhu [2 ]
Jiang, Xiaodan [1 ]
机构
[1] Southern Med Univ, Zhujiang Hosp,Dept Neurosurg, Guangdong Prov Key Lab Brain Funct Repair & Regen, Natl Key Clin Specialty,Neurosurg Inst Guangdong, Guangzhou 510282, Guangdong, Peoples R China
[2] Yangzhou Univ, Clin Med Coll, Dept Neurosurg, Yangzhou 225001, Jiangsu, Peoples R China
关键词
Stem cell; Immunology; Cell therapy; FOCAL CEREBRAL-ISCHEMIA; ACTIVATION; PROLIFERATION;
D O I
10.1016/j.brainres.2014.05.041
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Human amniotic membrane-derived mesenchymal stem cells (AMSCs) are considered a novel and promising source of stem cells for cell replacement-based therapy. Current research is mostly limited to investigating the cellular differentiation potential of AMSCs, while few have focused on their immunosuppressive properties. This study is aimed at exploring and evaluating the immunosuppressive effect of human AMSCs on the viability and migratory properties of microglia. We found, from results of cell viability assays, that AMSCs can reduce the activity of inflammatory cells by secreting nitric oxide (NO). Also, based on results from wound healing and transwell migration assays, we show that AMSCs can inhibit the migration of human microglia as well as the mouse microglial cell line BV2, suggesting that they have the ability to inhibit the recruitment of certain immune cells to injury sites. Furthermore, we found that NO contributes significantly to this inhibitory effect. Our study provides evidence that human AMSCs can have detrimental effects on the viability and migration of microglia, through secretion of NO. This mechanism may contribute to anti-inflammatory processes in the central nervous system. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:1 / 9
页数:9
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