Effects of Neural Progenitor Cells on Sensorimotor Recovery and Endogenous Repair Mechanisms After Photothrombotic Stroke
Effects of Neural Progenitor Cells on Sensorimotor Recovery and Endogenous Repair Mechanisms After Photothrombotic Stroke
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DOI：
10.1161/strokeaha.110.599282
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发表时间：
2011-06-01
期刊：
影响因子：
8.3
通讯作者：
Schaebitz, Wolf-Ruediger
中科院分区：
文献类型：
--
作者：
Minnerup, Jens;Kim, Jeong Beom;Schaebitz, Wolf-Ruediger
背景和目的-静脉注射神经祖细胞（NPC）治疗被证明可以改善实验性卒中后的功能恢复。然而，到目前为止，其基本机制尚未完全了解。在这里，我们研究了全身NPC移植对内源性神经发生和树突可塑性的宿主neurons. Methods二十四小时后，光血栓缺血，成年大鼠接受5万NPC或安慰剂静脉注射的影响。缺血后每周进行一次行为测试，直至4周。内源性神经发生，树突的长度，和树突状分支的皮质锥体细胞和小胶质细胞activationwere quantited.Results-NPC治疗导致了显着改善的感觉运动功能测定的粘合剂去除试验。与安慰剂治疗相比，NPC移植后树突长度和分支点数量显著增加，而内源性神经发生减少。内源性神经发生减少与激活的小胶质细胞的数量增加。结论-我们的研究结果表明，增加树突状细胞的可塑性可能是NPC诱导的功能恢复的结构基础。NPC治疗后内源性神经发生的减少似乎是由小胶质细胞活化介导的。（中风。2011; 42：1757-1763.）
Background and Purpose-Intravenous neural progenitor cell (NPC) treatment was shown to improve functional recovery after experimental stroke. The underlying mechanisms, however, are not completely understood so far. Here, we investigated the effects of systemic NPC transplantation on endogenous neurogenesis and dendritic plasticity of host neurons.Methods-Twenty-four hours after photothrombotic ischemia, adult rats received either 5 million NPC or placebo intravenously. Behavioral tests were performed weekly up to 4 weeks after ischemia. Endogenous neurogenesis, dendritic length, and dendritic branching of cortical pyramid cells and microglial activation were quantified.Results-NPC treatment led to a significantly improved sensorimotor function measured by the adhesive removal test. The dendritic length and the amount of branch points were significantly increased after NPC transplantation, whereas endogenous neurogenesis was decreased compared to placebo therapy. Decreased endogenous neurogenesis was associated with an increased number of activated microglial cells.Conclusions-Our findings suggest that an increased dendritic plasticity might be the structural basis of NPC-induced functional recovery. The decreased endogenous neurogenesis after NPC treatment seems to be mediated by microglial activation. (Stroke. 2011; 42: 1757-1763.)