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蛋白质二硫键异构酶A6通过与痉挛蛋白相互作用促进受损神经的修复。

Protein disulfide isomerase A6 promotes the repair of injured nerve through interactions with spastin.

作者信息

Luo Jianxian, Xie Min, Peng Cheng, Ma Yanming, Wang Ke, Lin Gengxiong, Yang Hua, Chen Tianjun, Liu Qiuling, Zhang Guowei, Lin Hongsheng, Ji Zhisheng

机构信息

Department of Orthopedics, The First Affiliated Hospital, Jinan University, Guangzhou, China.

Department of Orthopedics, Zhuhai Hospital Affiliated with Jinan University (Zhuhai People's Hospital), Zhuhai, China.

出版信息

Front Mol Neurosci. 2022 Aug 24;15:950586. doi: 10.3389/fnmol.2022.950586. eCollection 2022.

Abstract

The maintenance of appropriate endoplasmic reticulum (ER) homeostasis is critical to effective spinal cord injury (SCI) repair. In previous reports, protein disulfide isomerase A6 (PDIA6) demonstrated to serve as a reversible functional modulator of ER stress responses, while spastin can coordinate ER organization through the modulation of the dynamic microtubule network surrounding this organelle. While both PDIA6 and spastin are thus important regulators of the ER, whether they interact with one another for SCI repair still needs to be determined. Here a proteomics analysis identified PDIA6 as being related to SCI repair, and protein interaction mass spectrometry further confirmed the ability of PDIA6 and spastin to interact with one another. Pull-down and co-immunoprecipitation assays were further performed to validate and characterize the interactions between these two proteins. The RNAi-based knockdown of PDIA6 in COS-7 cells inhibited the activity of spastin-dependent microtubule severing. PDIA6 was also found to promote injured neuron repair, while spastin knockdown reversed this reparative activity. Together, these results thus confirm that PDIA6 and spastin function together as critical mediators of nerve repair, highlighting their potential value as validated targets for efforts to promote SCI repair.

摘要

维持适当的内质网(ER)稳态对于有效的脊髓损伤(SCI)修复至关重要。在先前的报道中,蛋白质二硫键异构酶A6(PDIA6)被证明是内质网应激反应的可逆功能调节剂,而痉挛蛋白可以通过调节围绕该细胞器的动态微管网络来协调内质网的组织。因此,虽然PDIA6和痉挛蛋白都是内质网的重要调节因子,但它们是否相互作用以促进SCI修复仍有待确定。在这里,蛋白质组学分析确定PDIA6与SCI修复有关,蛋白质相互作用质谱进一步证实了PDIA6和痉挛蛋白相互作用的能力。进一步进行了下拉和共免疫沉淀试验,以验证和表征这两种蛋白质之间的相互作用。在COS-7细胞中基于RNA干扰敲低PDIA6抑制了痉挛蛋白依赖性微管切断的活性。还发现PDIA6促进受损神经元的修复,而敲低痉挛蛋白则逆转了这种修复活性。总之,这些结果证实PDIA6和痉挛蛋白共同作为神经修复的关键介质,突出了它们作为促进SCI修复努力的有效靶点的潜在价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6598/9449696/7fb4c54fd9a7/fnmol-15-950586-g001.jpg

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