scholarly journals Controlled release of neurotrophin-3 from fibrin-based tissue engineering scaffolds enhances neural fiber sprouting following subacute spinal cord injury

2009 ◽  
Vol 104 (6) ◽  
pp. 1207-1214 ◽  
Author(s):  
Philip J. Johnson ◽  
Stanley R. Parker ◽  
Shelly E. Sakiyama-Elbert
2019 ◽  
Vol 14 (9) ◽  
pp. 887-898
Author(s):  
Zhanjun Ma ◽  
Yubao Lu ◽  
Yang Yang ◽  
Jing Wang ◽  
Xuewen Kang

Spinal cord injury (SCI) is one of the leading causes of global disability. However, there are currently no effective clinical treatments for SCI. Repair of SCI is essential but poses great challenges. As a comprehensive treatment program combining biological scaffolds, seed cells and drugs or biological factors, tissue engineering has gradually replaced the single transplantation approach to become a focus of research that brings new opportunities for the clinical treatment of SCI.


2004 ◽  
Vol 98 (2) ◽  
pp. 281-294 ◽  
Author(s):  
Sara J Taylor ◽  
John W McDonald ◽  
Shelly E Sakiyama-Elbert

2022 ◽  
Author(s):  
Jianwu Dai ◽  
Yunlong Zou ◽  
Yanyun Yin ◽  
Zhifeng Xiao ◽  
Yannan Zhao ◽  
...  

Numerous studies have indicated that microgravity induces various changes in the cellular functions of neural stem cells (NSCs), and the use of microgravity to culture tissue engineering seed cells for...


2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Qi Han ◽  
Josue D. Ordaz ◽  
Nai-Kui Liu ◽  
Zoe Richardson ◽  
Wei Wu ◽  
...  

AbstractLocomotor function, mediated by lumbar neural circuitry, is modulated by descending spinal pathways. Spinal cord injury (SCI) interrupts descending projections and denervates lumbar motor neurons (MNs). We previously reported that retrogradely transported neurotrophin-3 (NT-3) to lumbar MNs attenuated SCI-induced lumbar MN dendritic atrophy and enabled functional recovery after a rostral thoracic contusion. Here we functionally dissected the role of descending neural pathways in response to NT-3-mediated recovery after a T9 contusive SCI in mice. We find that residual projections to lumbar MNs are required to produce leg movements after SCI. Next, we show that the spared descending propriospinal pathway, rather than other pathways (including the corticospinal, rubrospinal, serotonergic, and dopaminergic pathways), accounts for NT-3-enhanced recovery. Lastly, we show that NT-3 induced propriospino-MN circuit reorganization after the T9 contusion via promotion of dendritic regrowth rather than prevention of dendritic atrophy.


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