A subpopulation of endothelial progenitor cells with low aldehyde dehydrogenase activity attenuates acute ischemic brain injury in rats

被引：26
作者：
Nakamura, Kazuhiro [1 ]
Tsurushima, Hideo [1 ]
Marushima, Aiki [1 ]
Nagano, Masumi [2 ]
Yamashita, Toshiharu [2 ]
Suzuki, Kensuke [3 ]
Ohneda, Osamu [2 ]
Matsumura, Akira [1 ]
机构：
[1] Univ Tsukuba, Fac Med, Dept Neurosurg, Tsukuba, Ibaraki 3058575, Japan
[2] Univ Tsukuba, Fac Med, Dept Regenerat Med & Stem Cell Biol, Tsukuba, Ibaraki 3058575, Japan
[3] Dokkyo Med Univ, Koshigaya Hosp, Dept Neurosurg, Koshigaya, Saitama 3438555, Japan
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2012年 / 418卷 / 01期
关键词：
Endothelial progenitor cells; Aldehyde dehydrogenase activity; Cell transplantation therapy; SDF-1; CXCR4; FOCAL CEREBRAL-ISCHEMIA; CXC CHEMOKINE PBSF/SDF-1; UMBILICAL-CORD BLOOD; BONE-MARROW; DOWN-REGULATION; RECEPTOR CXCR4; STROKE; TRANSPLANTATION; STEM; MICE;
D O I：
10.1016/j.bbrc.2011.12.139
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Previous studies have examined the therapeutic effect of endothelial progenitor cells (EPCs) during the chronic phase of cerebral infarction in rats; however, few studies have investigated the effects of EPCs during the acute phase of infarction. In this study, we evaluated the therapeutic effect of EPCs with low aldehyde dehydrogenase activity (Aide-Low EPCs) in rats with acute cerebral infarction, and our results provide insight that may help to identify a therapeutic mechanism of EPCs for acute cerebral infarction. The administration of Alde-Low EPCs into rats with acute cerebral infarction results in the accumulation and migration of the Aide-Low EPCs into the infarct area and the subsequent decrease of infarct volume. Moreover, we found that the stromal cell-derived factor-1 (SDF-1) and CXC chemokine receptor 4 (CXCR4) signaling pathway may regulate the accumulation of Aide-Low EPCs. The transplantation of Aide-Low EPCs may represent a potential treatment strategy for acute cerebral infarction. (C) 2012 Elsevier Inc. All rights reserved.
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收藏
页码：87 / 92
页数：6
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