Doeppner Thorsten R, Traut Viktorija, Heidenreich Alexander, Kaltwasser Britta, Bosche Bert, Bähr Mathias, Hermann Dirk M
Department of Neurology, University of Duisburg-Essen Medical School, Essen, Germany.
Regenerative and Restorative Medical Research Center, Istanbul Medipol University, Istanbul, Turkey.
Mol Neurobiol. 2017 Mar;54(2):1531-1540. doi: 10.1007/s12035-016-9748-y. Epub 2016 Feb 9.
Adult neural progenitor cells (NPCs) induce post-ischemic long-term neuroprotection and brain remodeling by releasing of survival- and plasticity-promoting mediators. To evaluate whether secreted factors may mimic neuroprotective and restorative effects of NPCs, we exposed male C57BL6 mice to focal cerebral ischemia and intravenously applied conditioned medium (CM) derived from subventricular zone NPCs. CM dose-dependently reduced infarct volume and brain leukocyte infiltration after 48 h when delivered up to 12 h after focal cerebral ischemia. Neuroprotection persisted in the post-acute stroke phase yielding enhanced neurological recovery that lasted throughout the 28-day observation period. Increased Bcl-2, phosphorylated Akt and phosphorylated STAT-3 abundance, and reduced caspase-3 activity and Bax abundance were noted in ischemic brains of CM-treated mice at 48 h post-stroke, indicative of enhanced cell survival signaling. Long-term neuroprotection was associated with increased brain glial cell line-derived neurotrophic factor (GDNF) and vascular endothelial growth factor (VEGF) concentrations at 28 days resulting in increased neurogenesis and angiogenesis. The observation that NPC-derived CM induces sustained neuroprotection and neurological recovery suggests that cell transplantation may be dispensable when secreted factors are instead administered.
成年神经祖细胞(NPCs)通过释放促进存活和可塑性的介质诱导缺血后长期神经保护和脑重塑。为了评估分泌因子是否可以模拟NPCs的神经保护和恢复作用,我们将雄性C57BL6小鼠暴露于局灶性脑缺血,并静脉注射源自脑室下区NPCs的条件培养基(CM)。当在局灶性脑缺血后12小时内给予CM时,在48小时后CM剂量依赖性地减少了梗死体积和脑白细胞浸润。神经保护作用在急性中风后阶段持续存在,导致神经功能恢复增强,这种增强在整个28天的观察期内持续。在中风后48小时,在接受CM治疗的小鼠的缺血脑中,观察到Bcl-2、磷酸化Akt和磷酸化STAT-3丰度增加,以及caspase-3活性和Bax丰度降低,这表明细胞存活信号增强。长期神经保护作用与28天时脑胶质细胞源性神经营养因子(GDNF)和血管内皮生长因子(VEGF)浓度增加有关,导致神经发生和血管生成增加。NPCs来源的CM诱导持续神经保护和神经功能恢复这一观察结果表明,当改为施用分泌因子时,细胞移植可能是不必要的。