NDLI: Ameliorative Effects of p75NTR-ED-Fc on Axonal Regeneration and Functional Recovery in Spinal Cord-Injured Rats

Content Provider	Springer Nature Link
Author	Wang, Yong Tang Lu, Xiu Min Zhu, Feng Huang, Peng Yu, Ying Long, Zai Yun Wu, Ya Min
Copyright Year	2014
Abstract	As a co-receptor of Nogo-66 receptor (NgR) and a critical receptor for paired immunoglobulin-like receptor (PirB), p75 neurotrophin receptor (p75NTR) mediates the inhibitory effects of myelin-associated inhibitors on axonal regeneration after spinal cord injury. Therefore, the p75NTR antagonist, such as recombinant p75NTR protein or its homogenates may block the inhibitory effects of myelin and promote the axonal regeneration and functional recovery. The purposes of this study are to subclone and express the extracellular domain gene of human p75NTR with IgG-Fc (hp75NTR-ED-Fc) in prokaryotic expression system and investigate the effects of the recombinant protein on axonal regeneration and functional recovery in spinal cord-injured rats. The hp75NTR-ED-Fc coding sequence was amplified from pcDNA-hp75NTR-ED-Fc by polymerase chain reaction (PCR) and subcloned into vector pET32a (+), then the effects of the purified recombinant protein on neurite outgrowth of dorsal root ganglion (DRG) neurons cultured with myelin-associated glycoprotein (MAG) were determined, and the effects of the fusion protein on axonal regeneration, functional recovery, and its possible mechanisms in spinal cord-injured rats were further investigated. The results indicated that the purified infusion protein could promote neurite outgrowth of DRG neurons, promote axonal regeneration and functional recovery, and decrease RhoA activation in spinal cord-injured rats. Taken together, the findings revealed that p75NTR still may be a potential and novel target for therapeutic intervention for spinal cord injury and that the hp75NTR-ED-Fc fusion protein treatment enhances functional recovery by limiting tissue loss and stimulating axonal growth in spinal cord-injured rats, which may result from decreasing the activation of RhoA.
Starting Page	1821
Ending Page	1834
Page Count	14
File Format	PDF
ISSN	08937648
Journal	Molecular Neurobiology
Volume Number	52
Issue Number	3
e-ISSN	15591182
Language	English
Publisher	Springer US
Publisher Date	2014-11-15
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	p75NTR-ED-Fc Neurite outgrowth Axonal regeneration Functional recovery Spinal cord injury Neurosciences Neurobiology Cell Biology Neurology
Content Type	Text
Resource Type	Article
Subject	Neurology Cellular and Molecular Neuroscience

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