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CLC number: R493

On-line Access: 2016-07-06

Received: 2015-12-02

Revision Accepted: 2016-03-31

Crosschecked: 2016-06-23

Cited: 1

Clicked: 1446

Citations:  Bibtex RefMan EndNote GB/T7714

 ORCID:

Qing-ping Tang

http://orcid.org/0000-0002-8729-1490

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Journal of Zhejiang University SCIENCE B 2016 Vol.17 No.7 P.493-502

http://doi.org/10.1631/jzus.B1500297


STAT3 signal that mediates the neural plasticity is involved in willed-movement training in focal ischemic rats


Author(s):  Qing-ping Tang, Qin Shen, Li-xiang Wu, Xiang-ling Feng, Hui Liu, Bei Wu, Xiao-song Huang, Gai-qing Wang, Zhong-hao Li, Zun-jing Liu

Affiliation(s):  Department of Rehabilitation, Brain Hospital of Hunan Province, Hunan University of Chinese Medicine, Changsha 410007, China; more

Corresponding email(s):   liuzunjing@163.com

Key Words:  Motor training, Signal transducer and activator of transcription 3 (STAT3), Brain-derived neurotrophic factor (BDNF), Protein interacting with C kinase 1 (PICK1), Neural plasticity


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Qing-ping Tang, Qin Shen, Li-xiang Wu, Xiang-ling Feng, Hui Liu, Bei Wu, Xiao-song Huang, Gai-qing Wang, Zhong-hao Li, Zun-jing Liu. STAT3 signal that mediates the neural plasticity is involved in willed-movement training in focal ischemic rats[J]. Journal of Zhejiang University Science B, 2016, 17(7): 493-502.

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author="Qing-ping Tang, Qin Shen, Li-xiang Wu, Xiang-ling Feng, Hui Liu, Bei Wu, Xiao-song Huang, Gai-qing Wang, Zhong-hao Li, Zun-jing Liu",
journal="Journal of Zhejiang University Science B",
volume="17",
number="7",
pages="493-502",
year="2016",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B1500297"
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%0 Journal Article
%T STAT3 signal that mediates the neural plasticity is involved in willed-movement training in focal ischemic rats
%A Qing-ping Tang
%A Qin Shen
%A Li-xiang Wu
%A Xiang-ling Feng
%A Hui Liu
%A Bei Wu
%A Xiao-song Huang
%A Gai-qing Wang
%A Zhong-hao Li
%A Zun-jing Liu
%J Journal of Zhejiang University SCIENCE B
%V 17
%N 7
%P 493-502
%@ 1673-1581
%D 2016
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1500297

TY - JOUR
T1 - STAT3 signal that mediates the neural plasticity is involved in willed-movement training in focal ischemic rats
A1 - Qing-ping Tang
A1 - Qin Shen
A1 - Li-xiang Wu
A1 - Xiang-ling Feng
A1 - Hui Liu
A1 - Bei Wu
A1 - Xiao-song Huang
A1 - Gai-qing Wang
A1 - Zhong-hao Li
A1 - Zun-jing Liu
J0 - Journal of Zhejiang University Science B
VL - 17
IS - 7
SP - 493
EP - 502
%@ 1673-1581
Y1 - 2016
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1500297


Abstract: 
Willed-movement training has been demonstrated to be a promising approach to increase motor performance and neural plasticity in ischemic rats. However, little is known regarding the molecular signals that are involved in neural plasticity following willed-movement training. To investigate the potential signals related to neural plasticity following willed-movement training, littermate rats were randomly assigned into three groups: middle cerebral artery occlusion, environmental modification, and willed-movement training. The infarct volume was measured 18 d after occlusion of the right middle cerebral artery. Reverse transcription-polymerase chain reaction (PCR) and immunofluorescence staining were used to detect the changes in the signal transducer and activator of transcription 3 (STAT3) mRNA and protein, respectively. A chromatin immunoprecipitation was used to investigate whether STAT3 bound to plasticity-related genes, such as brain-derived neurotrophic factor (BDNF), synaptophysin, and protein interacting with C kinase 1 (PICK1). In this study, we demonstrated that STAT3 mRNA and protein were markedly increased following 15-d willed-movement training in the ischemic hemispheres of the treated rats. STAT3 bound to BDNF, PICK1, and synaptophysin promoters in the neocortical cells of rats. These data suggest that the increased STAT3 levels after willed-movement training might play critical roles in the neural plasticity by directly regulating plasticity-related genes.

调控神经可塑性的STAT3在意向性运动疗法干预后局灶性脑缺血大鼠中的表达

目的:探讨意向性运动疗法干预后与神经可塑性相关的信号通路。
创新点:首次发现意向性运动疗法干预后信号传导与转录激活因子3(STAT3)表达增高,以及STAT3直接调控神经可塑性相关基因。
方法:将大脑中动脉梗死(MCAO)模型大鼠随机分为MCAO组、环境改变组和意向性运动疗法组。18天后测量三组大鼠的脑梗死面积。应用逆转录聚合酶链反应(RT-PCR)和荧光免疫染色法分别检测STAT3的基因和蛋白的表达;应用染色质免疫共沉淀检测STAT3是否绑定脑源性神经营养因子(BDNF)、突触素以及蛋白激酶Cα相互作用蛋白1(PICK1)。
结论:研究结果显示:意向性运动疗法干预15天后,STAT3的基因与蛋白均增高;STAT3绑定皮层神经元BDNFPICK1和突触素的启动子区;意向性运动干预后STAT3的升高可能与神经可塑性相关。

关键词:运动训练;信号传导与转录激活因子3(STAT3);脑源性神经营养因子(BDNF);突触素;蛋白激酶Cα相互作用蛋白1(PICK1);神经可塑性

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