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| STAT3 signal that mediates the neural plasticity is involved in willed-movement training in focal ischemic rats |
| 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 |
| Department of Rehabilitation, Brain Hospital of Hunan Province, Hunan University of Chinese Medicine, Changsha 410007, China; Department of Physiology, School of Basic Medical Sciences, Central South University, Changsha 410078, China; Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, China; Cancer Research Institute, Xiangya School of Medicine, Central South University, Changsha 410078, China; Department of Otolaryngology, Xiangya Hospital, Central South University, Changsha 410008, China; Department of Neurology, Brain Hospital of Hunan Province, Hunan University of Chinese Medicine, Changsha 410007, China; Department of Neurology, the Second Hospital, Shanxi Medical University, Taiyuan 030001, China; Department of Neurology, China-Japan Friendship Hospital, Beijing 100029, China |
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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.
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Received: 02 December 2015
Published: 06 July 2016
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Cite this article:
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. Journal of Zhejiang University-SCIENCE B (Biomedicine & Biotechnology), 2016, 17(7): 493-502.
URL:
http://www.zjujournals.com/xueshu/zjus-b/10.1631/jzus.B1500297 OR http://www.zjujournals.com/xueshu/zjus-b/Y2016/V17/I7/493
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