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Neural Plasticity
Volume 2017, Article ID 1621629, 22 pages
Research Article

AAV-KLF7 Promotes Descending Propriospinal Neuron Axonal Plasticity after Spinal Cord Injury

1Department of Anatomy, Basic Medical College, China Medical University, Shenyang 110122, China
2Department of Anatomy, Mudanjiang College of Medicine, Mudanjiang 157011, China
3Department of Pharmacy, Mudanjiang College of Medicine, Mudanjiang 157011, China
4Department of Pathology, Mudanjiang College of Medicine, Mudanjiang 157011, China
5Spinal Cord and Brain Injury Research Group, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA

Correspondence should be addressed to Ying Wang; moc.361@422077gnawgniy and Zhen-Yu Wang; nc.ude.umc.liam@gnawyz

Received 13 March 2017; Revised 27 May 2017; Accepted 12 June 2017; Published 13 August 2017

Academic Editor: Malgorzata Kossut

Copyright © 2017 Wen-Yuan Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


DPSN axons mediate and maintain a variety of normal spinal functions. Unsurprisingly, DPSN tracts have been shown to mediate functional recovery following SCI. KLF7 could contribute to CST axon plasticity after spinal cord injury. In the present study, we assessed whether KLF7 could effectively promote DPSN axon regeneration and synapse formation following SCI. An AAV-KLF7 construct was used to overexpress KLF7. In vitro, KLF7 and target proteins were successfully elevated and axonal outgrowth was enhanced. In vivo, young adult C57BL/6 mice received a T10 contusion followed by an AAV-KLF7 injection at the T7–9 levels above the lesion. Five weeks later, overexpression of KLF7 was expressed in DPSN. KLF7 and KLF7 target genes (NGF, TrkA, GAP43, and P0) were detectably increased in the injured spinal cord. Myelin sparring at the lesion site, DPSN axonal regeneration and synapse formation, muscle weight, motor endplate morphology, and functional parameters were all additionally improved by KLF7 treatment. Our findings suggest that KLF7 promotes DPSN axonal plasticity and the formation of synapses with motor neurons at the caudal spinal cord, leading to improved functional recovery and further supporting the potential of AAV-KLF7 as a therapeutic agent for spinal cord injury.