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| Hsp22对SCA3/MJD转基因果蝇的神经保护作用研究 | |
| 引用本文： | 李清华,江泓,易继平,廖书胜,沈 璐,潘 乾,夏 昆,唐北沙. Hsp22对SCA3/MJD转基因果蝇的神经保护作用研究[J]. 生物化学与生物物理进展, 2008, 35(12): 1430-1436 |
| 作者姓名： | 李清华 江泓 易继平 廖书胜 沈 璐 潘 乾 夏 昆 唐北沙 |
| 作者单位： | 1. 中南大学湘雅医院神经内科,长沙,410008;唯林医学院附属医院神经内科,桂林,541001 2. 中南大学湘雅医院神经内科,长沙,410008;中南大学神经退行性疾病研究中心,长沙,410008 3. 中南大学湘雅医院神经内科,长沙,410008 4. 中南大学医学遗传学国家重点实验室,长沙,410008 5. 中南大学湘雅医院神经内科,长沙,410008;中南大学神经退行性疾病研究中心,长沙,410008;中南大学医学遗传学国家重点实验室,长沙,410008 |
| 基金项目： | 国家高技术研究发展计划项目(863)(2004AA227040), 国家“十一五”支撑计划项目(2006BA105A07), 国家“十五”攻关计划项目(2004BA720A03), 国家自然科学基金项目(30871354, 30710303061, 30400262)和湖南省自然科学基金重点项目(08JJ3048). |
| 摘 要： | 为了探讨Hsp22在SCA3/MJD发病机制中的作用．选用GMR-GAL4和elav-GAL4驱动子，利用经典的GAL4-UAS系统，将含有78个CAG重复扩增的ataxin-3蛋白片段(MJDtr-Q78)分别在果蝇眼睛和神经系统选择性表达，构建GMR-GAL4/UAS和elav-GAL4/UAS系统SCA3/MJD转基因果蝇模型， 然后利用遗传学方法和热休克反应使Hsp22在SCA3/ MJD转基因果蝇眼睛和神经系统以不同水平过表达．结果表明，Hsp22过表达显著抑制了MJDtr-Q78蛋白的神经毒性，果蝇眼睛视网膜光感受神经元变性明显缓解，果蝇存活能力也显著提高．Hsp22对SCA3/MJD具有保护作用，增强Hsp22表达对SCA3/MJD可能是一种潜在的治疗方法． |
| 关 键 词： | 遗传性脊髓小脑性共济失调3型，ataxin-3，Hsp22，转基因果蝇模型，神经保护 |
| 收稿时间： | 2008-07-11 |
| 修稿时间： | 2008-10-09 |
Research on Neuroprotective Role of Hsp22 in SCA3/MJD Transgenic Drosophila Models |
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| LI Qing-Hu,JIANG Hong,YI Ji-Ping,LIAO Shu-Sheng,SHEN Lu,PAN Qian,XIA Kun and TANG Bei-Sha. Research on Neuroprotective Role of Hsp22 in SCA3/MJD Transgenic Drosophila Models[J]. Progress In Biochemistry and Biophysics, 2008, 35(12): 1430-1436 | |
| Authors: | LI Qing-Hu JIANG Hong YI Ji-Ping LIAO Shu-Sheng SHEN Lu PAN Qian XIA Kun TANG Bei-Sha |
| Affiliation: | Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, China;Department of Neurology, Affiliated Hospital of Guilin Medical University, Guilin 541001, China;Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, China;Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, China;Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, China;Neurodegenerative Disorders Research Center, Central South University, Changsha 410008, China;National Laboratory of Medical Genetics of China, Central South University, Changsha 410008, China;National Laboratory of Medical Genetics of China, Central South University, Changsha 410008, China;Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, China;Neurodegenerative Disorders Research Center, Central South University, Changsha 410008, China;National Laboratory of Medical Genetics of China, Central South University, Changsha 410008, China |
| Abstract: | To confer the influence of Hsp22 on pathogenesis of SCA3/MJD. GMR-GAL4 and elav-GAL4 system SCA3/MJD transgenic Drosophila models were constructed by using the promoter GMR-GAL4 and elav-GAL4 which drive target selective gene expression in developing eyes and neurons, respectively. Then, Hsp22 protein was overexpressed in SCA3/MJD transgenic Drosophila models at different levels by genetic methods and heat shock reaction. Overexpression of endogen Drosophila Hsp22 can notably suppress the neurotoxicity of MJDtr-Q78 protein, and the level of Hsp22 expression was in consistent with rehabilitation for neurodegeneration of Drosophila eyes, and extension of Drosophila lifespan. It is firstly confirmed that expression of Hsp22 protects the SCA3/MJD from neurodegeneration on Drosophila models, which might contribute to a potential therapeutic effect on SCA3/MJD. |
| Keywords: | SCA3 ataxin-3 Hsp22 transgenic Drosophila models neuroprotection |
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