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SNAP25 Ameliorates Sensory Deficit in Rats with Spinal Cord Transection |
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| Authors: | Wei Wang Fang Wang Jia Liu Wei Zhao Qi Zhao Mu He Bao-Jiang Qian Yang Xu Ran Liu Su-Juan Liu Wei Liu Jin Liu Xin-Fu Zhou Ting-Hua Wang |
| Institution: | 1. Department of Anesthesiology and Institute of Neurological Disease, Translation Neuroscience Center, The State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, People’s Republic of China 2. Institute of Neuroscience, Kunming Medical University, Kunming, 650031, People’s Republic of China 3. Department of Neurosurgery, Translation Neuroscience Center, West China Hospital, Sichuan University, Chengdu, 610041, People’s Republic of China 4. Department of Histology and Embryology, Sichuan University, Chengdu, 610041, People’s Republic of China 5. School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, SA, 5000, Australia |
| Abstract: | Spinal cord injury causes sensory loss below the level of lesion. Synaptosomal-associated protein 25 (SNAP25) is a t-SNARE protein essential for exocytosis and neurotransmitter release, but its role in sensory functional recovery has not been determined. The aim of the present study is therefore to investigate whether SNAP25 can promote sensory recovery. By 2D proteomics, we found a downregulation of SNAP25 and then constructed two lentiviral vectors, Lv-exSNAP25 and Lv-shSNAP25, which allows efficient and stable RNAi-mediated silencing of endogenous SNAP25. Overexpression of SNAP25 enhanced neurite outgrowth in vitro and behavior response to thermal and mechanical stimuli in vivo, while the silencing of SNAP25 had the opposite effect. These results suggest that SNAP25 plays a crucial role in sensory functional recovery following spinal cord injury (SCI). Our study therefore provides a novel target for the management of SCI for sensory dysfunction. |
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