AAV-KLF7 Promotes Descending Propriospinal Neuron Axonal Plasticity after Spinal Cord Injury
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 prom...
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| Format: | Article |
| Language: | English |
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Wiley
2017-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2017/1621629 |
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| author | Wen-Yuan Li Ying Wang Feng-Guo Zhai Ping Sun Yong-Xia Cheng Ling-Xiao Deng Zhen-Yu Wang |
| author_facet | Wen-Yuan Li Ying Wang Feng-Guo Zhai Ping Sun Yong-Xia Cheng Ling-Xiao Deng Zhen-Yu Wang |
| author_sort | Wen-Yuan Li |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-325f2b3a7c0b470d80012455fa168c0d |
| institution | Kabale University |
| issn | 2090-5904 1687-5443 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Neural Plasticity |
| spelling | doaj-art-325f2b3a7c0b470d80012455fa168c0d2025-02-03T01:26:30ZengWileyNeural Plasticity2090-59041687-54432017-01-01201710.1155/2017/16216291621629AAV-KLF7 Promotes Descending Propriospinal Neuron Axonal Plasticity after Spinal Cord InjuryWen-Yuan Li0Ying Wang1Feng-Guo Zhai2Ping Sun3Yong-Xia Cheng4Ling-Xiao Deng5Zhen-Yu Wang6Department of Anatomy, Basic Medical College, China Medical University, Shenyang 110122, ChinaDepartment of Anatomy, Mudanjiang College of Medicine, Mudanjiang 157011, ChinaDepartment of Pharmacy, Mudanjiang College of Medicine, Mudanjiang 157011, ChinaDepartment of Anatomy, Mudanjiang College of Medicine, Mudanjiang 157011, ChinaDepartment of Pathology, Mudanjiang College of Medicine, Mudanjiang 157011, ChinaSpinal Cord and Brain Injury Research Group, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USADepartment of Anatomy, Basic Medical College, China Medical University, Shenyang 110122, ChinaDPSN 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.http://dx.doi.org/10.1155/2017/1621629 |
| spellingShingle | Wen-Yuan Li Ying Wang Feng-Guo Zhai Ping Sun Yong-Xia Cheng Ling-Xiao Deng Zhen-Yu Wang AAV-KLF7 Promotes Descending Propriospinal Neuron Axonal Plasticity after Spinal Cord Injury Neural Plasticity |
| title | AAV-KLF7 Promotes Descending Propriospinal Neuron Axonal Plasticity after Spinal Cord Injury |
| title_full | AAV-KLF7 Promotes Descending Propriospinal Neuron Axonal Plasticity after Spinal Cord Injury |
| title_fullStr | AAV-KLF7 Promotes Descending Propriospinal Neuron Axonal Plasticity after Spinal Cord Injury |
| title_full_unstemmed | AAV-KLF7 Promotes Descending Propriospinal Neuron Axonal Plasticity after Spinal Cord Injury |
| title_short | AAV-KLF7 Promotes Descending Propriospinal Neuron Axonal Plasticity after Spinal Cord Injury |
| title_sort | aav klf7 promotes descending propriospinal neuron axonal plasticity after spinal cord injury |
| url | http://dx.doi.org/10.1155/2017/1621629 |
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