Administration of CD34+ cells after stroke enhances neurogenesis via angiogenesis in a mouse model
Administration of CD34+ cells after stroke enhances neurogenesis via angiogenesis in a mouse model
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DOI：
10.1172/jci200420622
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发表时间：
2004-08-01
影响因子：
15.9
通讯作者：
Matsuyama, T
中科院分区：
文献类型：
--
作者：
Taguchi, A;Soma, T;Matsuyama, T
导致中风和永久性神经元丧失的血栓闭塞性脑血管疾病是发病和死亡的重要原因。由于脑血管系统的独特性质和神经元组织的有限修复能力，很难设计出有效的脑缺血神经保护疗法。我们的结果表明，对48小时前中风的免疫功能低下的小鼠全身注射人脐带血来源的CD34(+)细胞，可诱导缺血区的新血管形成，并为神经元再生提供有利的环境。由于神经元祖细胞向受损区域的迁移增强，随后它们的成熟和功能恢复，被抗血管生成剂抑制的内源性神经发生被加速。我们的数据表明，CD34(+)细胞在直接或间接促进有利于缺血脑新生血管形成的环境中发挥重要作用，从而使神经元再生得以进行。
Thrombo-occlusive cerebrovascular disease resulting in stroke and permanent neuronal loss is an important cause of morbidity and mortality. Because of the unique properties of cerebral vasculature and the limited reparative capability of neuronal tissue, it has been difficult to devise effective neuroprotective therapies in cerebral ischemia. our results demonstrate that systemic administration of human cord blood-derived CD34(+) cells to immunocompromised mice subjected to stroke 48 hours earlier induces neovascularization in the ischemic zone and provides a favorable environment for neuronal regeneration. Endogenous neurogenesis, suppressed by an antiangiogenic agent, is accelerated as a result of enhanced migration of neuronal progenitor cells to the damaged area, followed by their maturation and functional recovery. Our data suggest an essential role for CD34(+) cells in promoting directly or indirectly an environment conducive to neovascularization of ischemic brain so that neuronal regeneration can proceed.