Pael-R基因未参与鱼藤酮诱导帕金森病细胞模型的变化

近来研究发现,环境毒素和遗传缺陷是引发帕金森病的分子机制。中国中南大学湘雅二医院邹婷所在团队前期研究发现,Parkin的作用底物之一Pael-R参与了Parkin基因突变引发多巴胺神经元凋亡的过程,但其是否也同时参与了环境毒素鱼藤酮引发多巴胺神经元凋亡的过程尚未知。在本次实验中探讨了在鱼藤酮诱导的帕金森模型中降低Pael-R的表达对模型细胞凋亡的影响,结果表明下调Pael-R表达后对帕金森病模型细胞的活率和凋亡没有影响。

SICENCE新闻发布 作者：邹婷 稿号：N20120504001 Pael-R基因未参与鱼藤酮诱导帕金森病细胞模型的变化

近来研究发现，环境毒素和遗传缺陷是引发帕金森病的分子机制。中国中南大学湘雅二医院邹婷所在团队前期研究发现，Parkin的作用底物之一Pael-R参与了Parkin基因突变引发多巴胺神经元凋亡的过程，但其是否也同时参与了环境毒素鱼藤酮引发多巴胺神经元凋亡的过程尚未知。在本次实验中探讨了在鱼藤酮诱导的帕金森模型中降低Pael-R的表达对模型细胞凋亡的影响，结果表明下调Pael-R表达后对帕金森病模型细胞的活率和凋亡没有影响，证实下调Pael-R基因的表达对鱼藤酮制作的帕金森病细胞模型没有保护作用。相关结果发表于《中国神经再生研究（英文版）》杂志2014年2月第4期。

Hoechst33258染色显示部分RNA干扰的帕金森病模型细胞细胞出现核固缩和核分裂

Article: " The Pael-R gene does not mediate the changes in rotenone-induced Parkinson’s disease model cells," by Ting Zou, Xiangqi Tang, Zhiling Huang, Niangui Xu, Zhiping Hu (Department of Neurology, Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China)

Zou T, Tang XQ, Huang ZL, Xu NG, Hu ZP. The Pael-R gene does not mediate the changes in rotenone-induced Parkinson’s disease model cells. Neural Regen Res. 2014;9(4):402-406.

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The Pael-R gene does not mediate the changes in rotenone-induced PD model cells

Currently, the pathogenesis of Parkinson’s disease is not entirely clear, but it has been generally considered to be the result of interactions among various genetic and environmental factors. Ting Zou and coworkers from Second Xiangya Hospital, Central South University in China previously found that Parkin mutation causes Parkin-associated endothelin receptor-like receptor (Pael-R) protein deposition, and the associated cytotoxicity leads to dopaminergic neuronal apoptosis. These researchers speculated that the Pael-R gene is possibly involved in the action of rotenone on cells. Therefore, they

investigated the role of the Pael-R gene in rotenone-induced Parkinson’s disease model cells using RNA interference. IN their recent study, Pael-R expression was decreased after RNA interference compared with the control group (no treatment) and the model group (rotenone treatment), while the rate of apoptosis and survival of dopaminergic cells did not differ

近来研究发现,环境毒素和遗传缺陷是引发帕金森病的分子机制。中国中南大学湘雅二医院邹婷所在团队前期研究发现,Parkin的作用底物之一Pael-R参与了Parkin基因突变引发多巴胺神经元凋亡的过程,但其是否也同时参与了环境毒素鱼藤酮引发多巴胺神经元凋亡的过程尚未知。在本次实验中探讨了在鱼藤酮诱导的帕金森模型中降低Pael-R的表达对模型细胞凋亡的影响,结果表明下调Pael-R表达后对帕金森病模型细胞的活率和凋亡没有影响。

SICENCE新闻发布 作者：邹婷 稿号：N20120504001

significantly between groups. Experimental findings, published in the Neural Regeneration Research (Vol. 9, No. 4, 2014), indicate that the Pael-R gene has no role in the changes in rotenone-induced Parkinson’s disease model cells.

In the RNA interference group, some cells showed nuclear condensation and division detected by Hoechst 33258 staining.

Article: " The Pael-R gene does not mediate the changes in rotenone-induced Parkinson’s disease model cells," by Ting Zou, Xiangqi Tang, Zhiling Huang, Niangui Xu, Zhiping Hu (Department of Neurology, Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China)

Zou T, Tang XQ, Huang ZL, Xu NG, Hu ZP. The Pael-R gene does not mediate the changes in rotenone-induced Parkinson’s disease model cells. Neural Regen Res. 2014;9(4):402-406.