CAS OpenIR  > 中科院上海应用物理研究所2011-2018年
Acupuncture promotes mTOR-independent autophagic clearance of aggregation-prone proteins in mouse brain
Tian, T; Sun, YH; Wu, HG; Pei, J; Zhang, J; Zhang, Y; Wang, L; Li, B; Wang, LH; Shi, JY; Hu, J; Fan, CH; Fan, CH (reprint author), Chinese Acad Sci, Shanghai Inst Appl Phys, Div Phys Biol, Shanghai 201800, Peoples R China.; Fan, CH (reprint author), Chinese Acad Sci, Shanghai Inst Appl Phys, CAS Key Lab Interfacial Phys & Technol, Bioimaging Ctr,Shanghai Synchrotron Radiat Facil, Shanghai 201800, Peoples R China.
2016
Source PublicationSCIENTIFIC REPORTS
ISSN2045-2322
Volume6Issue:-Pages:
Subtype期刊文献
AbstractAcupuncture has historically been practiced to treat medical disorders by mechanically stimulating specific acupoints with fine needles. Despite its well-documented efficacy, its biological basis remains largely elusive. In this study, we found that mechanical stimulation at the acupoint of Yanglingquan (GB34) promoted the autophagic clearance of alpha-synuclein (alpha-syn), a well known aggregation-prone protein closely related to Parkinson's disease (PD), in the substantia nigra par compacta (SNpc) of the brain in a PD mouse model. We found the protein clearance arose from the activation of the autophagylysosome pathway (ALP) in a mammalian target of rapamycin (mTOR)-independent approach. Further, we observed the recovery in the activity of dopaminergic neurons in SNpc, and improvement in the motor function at the behavior level of PD mice. Whereas acupuncture and rapamycin, a chemical mTOR inhibitor, show comparable a-syn clearance and therapeutic effects in the PD mouse model, the latter adopts a distinctly different, mTOR-dependent, autophagy induction process. Due to this fundamental difference, acupuncture may circumvent adverse effects of the rapamycin treatment. The newly discovered connection between acupuncture and autophagy not only provides a new route to understanding the molecular mechanism of acupuncture but also sheds new light on cost-effective and safe therapy of neurodegenerative diseases.
KeywordParkinsons-disease Neurodegenerative Disease Substantia-nigra Model Mptp Rapamycin Pathogenesis Toxicity Neurons Stress
DOI10.1038/srep19714
Indexed BySCI
Language英语
WOS IDWOS:000368789900002
Citation statistics
Cited Times:8[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.sinap.ac.cn/handle/331007/25642
Collection中科院上海应用物理研究所2011-2018年
Corresponding AuthorFan, CH (reprint author), Chinese Acad Sci, Shanghai Inst Appl Phys, Div Phys Biol, Shanghai 201800, Peoples R China.; Fan, CH (reprint author), Chinese Acad Sci, Shanghai Inst Appl Phys, CAS Key Lab Interfacial Phys & Technol, Bioimaging Ctr,Shanghai Synchrotron Radiat Facil, Shanghai 201800, Peoples R China.
Recommended Citation
GB/T 7714
Tian, T,Sun, YH,Wu, HG,et al. Acupuncture promotes mTOR-independent autophagic clearance of aggregation-prone proteins in mouse brain[J]. SCIENTIFIC REPORTS,2016,6(-):—.
APA Tian, T.,Sun, YH.,Wu, HG.,Pei, J.,Zhang, J.,...&Fan, CH .(2016).Acupuncture promotes mTOR-independent autophagic clearance of aggregation-prone proteins in mouse brain.SCIENTIFIC REPORTS,6(-),—.
MLA Tian, T,et al."Acupuncture promotes mTOR-independent autophagic clearance of aggregation-prone proteins in mouse brain".SCIENTIFIC REPORTS 6.-(2016):—.
Files in This Item: Download All
File Name/Size DocType Version Access License
Acupuncture promotes(1669KB)期刊论文作者接受稿开放获取CC BY-NC-SAView Download
Related Services
Recommend this item
Bookmark
Usage statistics
Export to Endnote
Google Scholar
Similar articles in Google Scholar
[Tian, T]'s Articles
[Sun, YH]'s Articles
[Wu, HG]'s Articles
Baidu academic
Similar articles in Baidu academic
[Tian, T]'s Articles
[Sun, YH]'s Articles
[Wu, HG]'s Articles
Bing Scholar
Similar articles in Bing Scholar
[Tian, T]'s Articles
[Sun, YH]'s Articles
[Wu, HG]'s Articles
Terms of Use
No data!
Social Bookmark/Share
File name: Acupuncture promotes mTOR-independent autophagic clearance of aggregation-prone proteins in mouse brain.pdf
Format: Adobe PDF
All comments (0)
No comment.
 

Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.