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作 者:刘光伟[1,2] 李瑛[1,2] 李昕[1,2] 李尧华[1,2] 于顺[1,2]
机构地区:[1]首都医科大学宣武医院神经生物学研究室 [2]北京市老年病医疗研究中心分子诊断实验室教育部神经变性病重点实验室,北京100053
出 处:《首都医科大学学报》2011年第6期759-763,共5页Journal of Capital Medical University
基 金:国家自然科学基金(81071014);国家重点基础发展计划(973项目)(2011CB504101);国家高技术研究发展计划(863计划)(2006AA02A408);北京市自然科学基金(7102076);北京市属高等学校人才强教计划(PHR200907113)~~
摘 要:目的研究人α-突触核蛋白(α-synuclein,α-syn)对MES23.5多巴胺能神经细胞突起生长的作用。方法 MES23.5细胞外添加α-syn蛋白,测定不同时间细胞突起的长度;免疫荧光双重标记法观察α-syn与β-微管蛋白之间的相互关系;ELISA方法检测细胞内β-微管蛋白含量。结果α-Syn处理组神经元突起的平均长度及β-微管蛋白的含量在培养1、4和24 h时均明显大于对照组;α-Syn的这一作用可被微管蛋白抑制剂秋水仙碱阻断;α-Syn与β-微管蛋白在细胞内共存。结论α-Syn具有促进MES23.5多巴胺能神经细胞突起生长的作用,该作用很可能通过影响微管蛋白的合成及微管的组装来完成。Objective To investigate the effect of α-synuclein(α-syn) on the neurite outgrowth of MES 23.5 dopaminergic cells. Methods The neurite length of MES 23.5 cells were measured at different time points after addition of recombinant human α-syn to the culture medium.Double immunofluorescent labeling was used to examine the co-localization of α-syn and β-tubulin in the cells.ELISA was applied to analyze the β-tubulin levels in the cells. Results The mean neurite length of the α-syn-treated cells was significantly longer than that of control neurons at 1 h,4 h and 24 h after addition of α-syn.The effect of α-syn on neurite outgrowth was reversed by β-tubulin inhibitor,colchicine.α-Syn and β-tubulin were shown to colocalize in the cells,and the levels of β-tubulin was higher in the α-syn-treated cells than in control cells. Conclusion α-Syn can promote neurite outgrowth of MES23.5 dopaminergic cells possibly by its effect on tubulin synthesis and microtubule assembly.
分 类 号:R338[医药卫生—人体生理学]
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