A subpopulation of endothelial progenitor cells with low aldehyde dehydrogenase activity attenuates acute ischemic brain injury in rats.
A subpopulation of endothelial progenitor cells with low aldehyde dehydrogenase activity attenuates acute ischemic brain injury in rats.
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DOI：
10.1016/j.bbrc.2011.12.139
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发表时间：
2012-02
影响因子：
3.1
通讯作者：
Kazuhiro Nakamura;H. Tsurushima;A. Marushima;Masumi Nagano;T. Yamashita;Kensuke Suzuki;O. Ohneda;A. Matsumura
中科院分区：
文献类型：
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作者：
Kazuhiro Nakamura;H. Tsurushima;A. Marushima;Masumi Nagano;T. Yamashita;Kensuke Suzuki;O. Ohneda;A. Matsumura
先前的研究已经检验了内皮祖细胞（EPC）在大鼠脑梗塞慢性期的治疗作用；然而，很少有研究调查 EPCs 在梗塞急性期的作用。在本研究中，我们评估了低乙醛脱氢酶活性的EPCs（Alde-Low EPCs）对急性脑梗死大鼠的治疗效果，我们的结果提供了见解，可能有助于确定EPCs治疗急性脑梗死的机制。将Alde-Low EPCs给予急性脑梗塞大鼠后，会导致Alde-Low EPCs在梗塞区域聚集并迁移至梗塞区域，从而导致梗塞体积减少。此外，我们发现基质细胞衍生因子1（SDF-1）和CXC趋化因子受体4（CXCR4）信号通路可能调节Alde-Low EPCs的积累。 Alde-Low EPCs 移植可能代表急性脑梗死的潜在治疗策略。
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 (Alde-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 Alde-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 Alde-Low EPCs. The transplantation of Alde-Low EPCs may represent a potential treatment strategy for acute cerebral infarction.