Sharma Rajesh K, Zhou Qihong, Netland Peter A
Department of Ophthalmology and Hamilton Eye Institute, University of Tennessee Health Science Center, 930 Madison Ave, Memphis, TN 38163, USA.
Brain Res. 2008 Dec 3;1243:19-26. doi: 10.1016/j.brainres.2008.08.025. Epub 2008 Aug 18.
Neural progenitor cells (NPCs) have drawn attention because they offer possible treatment for neurodegenerative disorders in the form of regenerative therapy or transplantation. NPCs adapt and change in response to the cues in the pathological environment. We assessed the effect of pre-exposure to non-cytotoxic levels of oxidative stress, a common pathogenic factor in a number of neurological disorders, on the cell viability and neurosphere morphology of NPCs derived from the periventricular zone of mice brain. Neural progenitor cell viability and neurosphere morphology (neurosphere number, size and chain migration) were assessed in response to cytotoxic levels of oxidative stress in the presence or absence of preconditioning with non-cytotoxic doses of hydrogen peroxide (H(2)O(2)). Preconditioning with non-cytotoxic levels of H(2)O(2) provided significant protection against subsequent exposure to lethal doses of H(2)O(2). Preconditioning also modulated alteration in the neurosphere morphology in response to oxidative stress. Oxidative stress increased chain migration and neurosphere size while decreasing neurosphere numbers, specially in the cultures that were preconditioned with higher doses of H(2)O(2). Non-cytotoxic exposure to oxidative stress can evoke endogenous cytoprotection in NPCs. Redox signaling plays a role in other cellular functions of NPCs, namely the chain migration of NPCs from neurospheres, perhaps as a result of its effect on cell differentiation.
神经祖细胞（NPCs）因其能以再生疗法或移植的形式为神经退行性疾病提供可能的治疗方法而备受关注。NPCs会根据病理环境中的信号进行适应和变化。我们评估了预先暴露于非细胞毒性水平的氧化应激（多种神经疾病中的常见致病因素）对源自小鼠脑室周围区域的NPCs的细胞活力和神经球形态的影响。在有或没有用非细胞毒性剂量的过氧化氢（H₂O₂）进行预处理的情况下，评估神经祖细胞活力和神经球形态（神经球数量、大小和链迁移）对细胞毒性水平氧化应激的反应。用非细胞毒性水平的H₂O₂进行预处理可显著保护细胞免受随后致死剂量H₂O₂的暴露。预处理还调节了氧化应激反应中神经球形态的改变。氧化应激增加了链迁移和神经球大小，同时减少了神经球数量，特别是在预先用较高剂量H₂O₂预处理的培养物中。非细胞毒性的氧化应激暴露可在NPCs中引发内源性细胞保护作用。氧化还原信号在NPCs的其他细胞功能中起作用，即NPCs从神经球的链迁移，这可能是其对细胞分化产生影响的结果。
