Transplantation with Hypoxia-preconditioned Mesenchymal Stem Cells Suppresses Brain Injury Caused by Cardiac Arrest-induced Global Cerebral Ischemia in Rats

被引:47
作者
Wang, Ji-wen [1 ,2 ]
Qiu, Yu-ru [1 ]
Fu, Yue [3 ]
Liu, Jun [4 ]
He, Zhi-jie [1 ]
Huang, Zi-tong [2 ,5 ]
机构
[1] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Intens Care Unit, Guangzhou, Guangdong, Peoples R China
[2] Sun Yat Sen Univ, Inst Cardiopulmonary Cerebral Resuscitat, Guangzhou, Guangdong, Peoples R China
[3] First Peoples Hosp Fo Shan, Dept Emergency Med, Fo Shan, Peoples R China
[4] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Neurol, Guangzhou, Guangdong, Peoples R China
[5] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Emergency Med, Guangzhou 510120, Guangdong, Peoples R China
关键词
hypoxia; mesenchymal stem cell; transplantation; cardiac arrest; cerebral ischemia; rat; migration; CXCR4; HIF; PI3K/AKT pathway; MARROW STROMAL CELLS; BONE-MARROW; PROGENITOR CELLS; SPINAL-CORD; IN-VITRO; MIGRATION; STROKE; ANGIOGENESIS; NEUROPROTECTION; CXCR4;
D O I
10.1002/jnr.24025
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Cardiac arrest-induced global cerebral ischemia is a main cause of neurological dysfunction in emergency medicine. Transplantation with bone marrow mesenchymal stem cells (MSCs) has been used in stroke models to repair the ischemic brain injury, but it is little studied in models with global cerebral ischemia. In the present study, a hypoxia precondition was used to improve the efficacy of MSC transplantation, given the low survival and migration rates and limited differentiation capacities of MSCs. We found that hypoxia can increase the expansion and migration of MSCs by activating the PI3K/AKT and hypoxia-inducible factor-1 alpha/CXC chemokine receptor-4 pathways. By using a cardiac arrest-induced global cerebral ischemic model in rats, we found that transplantation of hypoxia-preconditioned MSCs promoted the migration and integration of MSCs and decreased neuronal death and inflammation in the ischemic cortex. (C) 2017 Wiley Periodicals, Inc.
引用
收藏
页码:2059 / 2070
页数:12
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