Biodegradable polyurethane nerve guide conduits with different moduli influence axon regeneration in transected peripheral nerve injury

Author(s):  
Yanchao Wang ◽  
Rui-Chao Liang ◽  
Jingjing Lin ◽  
Jinlin Chen ◽  
qiao zhang ◽  
...  

Nerve guide conduits (NGCs) can replace autogenous nerve grafting in the treatment of peripheral nerve system (PNS) injury. However, the modulus of the polyurethane NGCs that affects the outcome of...

2021 ◽  
Vol 22 (13) ◽  
pp. 7217
Author(s):  
Arthur W. English ◽  
Ken Berglund ◽  
Dario Carrasco ◽  
Katharina Goebel ◽  
Robert E. Gross ◽  
...  

Functional recovery after peripheral nerve injury (PNI) is poor, mainly due to the slow and incomplete regeneration of injured axons. Experimental therapies that increase the excitability of the injured axons have proven remarkably successful in promoting regeneration, but their clinical applicability has been limited. Bioluminescent optogenetics (BL-OG) uses luminopsins, fusion proteins of light-generating luciferase and light-sensing ion channels that could be used to increase neuronal excitability if exposed to a suitable substrate. Excitatory luminopsins were expressed in motoneurons of transgenic mice and in wildtype mice transduced with adeno-associated viral vectors. Intraperitoneal administration of coelenterazine (CTZ), a known luciferase substrate, generated intense bioluminescence in peripheral axons. This bioluminescence increased motoneuron excitability. A single administration of CTZ immediately after sciatic nerve transection and repair markedly enhanced motor axon regeneration. Compound muscle action potentials were 3–4 times larger than controls by 4 weeks after injury. The results observed with transgenic mice were comparable to those of mice in which the luminopsin was expressed using viral vectors. Significantly more motoneurons had successfully reinnervated muscle targets four weeks after nerve injury in BL-OG treated mice than in controls. Bioluminescent optogenetics is a promising therapeutic approach to enhancing axon regeneration after PNI.


Author(s):  
Eun‐Hae Jang ◽  
Yun‐Hee Bae ◽  
Eun Mo Yang ◽  
Yunho Gim ◽  
Hyun‐Jun Suh ◽  
...  

Brain ◽  
2008 ◽  
Vol 131 (10) ◽  
pp. 2620-2631 ◽  
Author(s):  
Rubèn López-Vales ◽  
Xavier Navarro ◽  
Takao Shimizu ◽  
Constantinos Baskakis ◽  
George Kokotos ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Eun Jung Sohn ◽  
Hwan Tae Park

Schwann cells (SCs) contribute to nerve repair following injury; however, the underlying molecular mechanism is poorly understood. MicroRNAs (miRNAs), which are short noncoding RNAs, have been shown to play a role in neuronal disease. In this work, we show that miRNAs regulate the peripheral nerve system by modulating the migration and proliferation of SCs. Thus, miRNAs expressed in peripheral nerves may provide a potential therapeutic target for peripheral nerve injury or repair.


2020 ◽  
Vol 16 ◽  
pp. 174480692097191
Author(s):  
Yuanyuan Jia ◽  
Ming Zhang ◽  
Pei Li ◽  
Wenbo Tang ◽  
Yao Liu ◽  
...  

Little is known about the role of epigenetic modification in axon regeneration following peripheral nerve injury. The purpose of the present study was to investigate the role of long non-coding RNAs (lncRNAs) in the regulation of axon regeneration. We used bioinformatics to perform microarray analysis and screened total 476 lncRNAs and 129 microRNAs (miRNAs) of differentially expressed genes after sciatic nerve injury in mice. lncRNA-GM4208 and lncRNA-GM30085 were examined, and the changes in lncRNA expression in the L4–L6 dorsal root ganglia (DRG) following sciatic nerve crush injury were analyzed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The expression of lncRNAs in the DRG changed, indicating that they might be related to nerve regeneration in the DRG following peripheral nerve injury.


2020 ◽  
Author(s):  
Jesus P Camiña ◽  
Agustín Sánchez-Temprano ◽  
Saúl Leal-López ◽  
Jessica González-Sánchez ◽  
Carlos S. Mosteiro ◽  
...  

Abstract Background. Injuries to the peripheral nerve system are common conditions, with broad spectrum of symptoms depending on the impaired nerves and severity of damage. Although peripheral nervous system retains a remarkable ability for regeneration, it is estimated that less than ten percent of patients fully recover function after nerve injury and the available treatments remain suboptimal. Here, we identify a role for the obestatin/GPR39 system in the regulation of the Schwann cell plasticity as well as in the preservation of neuromuscular synapses in the course of nerve repair. Methods. Utilizing a compression model of sciatic nerve injury, axonotmesis, we assessed the obestatin-related regenerative response in the peripheral nerve system. The role of the obestatin/GPR39 system was further evaluated on immortalized rat Schwann cells, IFRS1, and the model of neuronal differentiation, PC12 cells. The interactions between SCs and neurons was evaluated using a co-culture system that combine the SC cell line IFRS1 and the NGF-primed PC12. Results. Obestatin signaling directs proliferation and migration of Schwann cells that sustain axonal regrowth and later remyelinate regenerated axons. We provide evidence supporting the preservation of skeletal muscle by the maintenance of neuromuscular synapses through the axonal regulation of calpain-calpastatin proteolytic system. This encompasses the control of skeletal muscle homeostasis by regulation of the ubiquitin proteasome system and the autophagy machinery. Conclusions. These results provide important insights into how the obestatin/GPR39 system promotes nerve repair through integration of multiple molecular cues of neuron-Schwann cells crosstalk aimed to promote axon growth and guide axons back to their targets.


Cell Reports ◽  
2021 ◽  
Vol 36 (10) ◽  
pp. 109666
Author(s):  
Yung-Chih Cheng ◽  
Andrew Snavely ◽  
Lee B. Barrett ◽  
Xuefei Zhang ◽  
Crystal Herman ◽  
...  

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