scholarly journals Neural crest stem cells protect spinal cord neurons from excitotoxic damage and inhibit glial activation by secretion of brain-derived neurotrophic factor

2018 ◽  
Vol 372 (3) ◽  
pp. 493-505 ◽  
Author(s):  
Nikos Schizas ◽  
N. König ◽  
B. Andersson ◽  
S. Vasylovska ◽  
J. Hoeber ◽  
...  
Stem Cells ◽  
2014 ◽  
Vol 32 (4) ◽  
pp. 829-843 ◽  
Author(s):  
Virginie Neirinckx ◽  
Dorothée Cantinieaux ◽  
Cécile Coste ◽  
Bernard Rogister ◽  
Rachelle Franzen ◽  
...  

Dose-Response ◽  
2020 ◽  
Vol 18 (1) ◽  
pp. 155932582091093
Author(s):  
YongLei Li ◽  
Hongchen Wang ◽  
Xiaofang Ding ◽  
Jiancheng Shen ◽  
Haitao Zhou ◽  
...  

Objective: To assess the effect as well as mechanism of bone marrow mesenchymal stem cells (BMSCs) modified by the human brain–derived neurotrophic factor gene combined with erythropoietin (EPO) in the treatment of acute spinal cord injury (SCI) in rats. Methods: The Brain-derived neurotrophic factor (BDNF) gene was transected by a virus vector. Rats with SCI were randomly split into following groups: The normal saline (NS) group, the EPO group, The Basso, Beattie, and Bresnahan scores, messenger RNA BDNF expression, and apoptosis rates were compared between the 4 groups at 1, 3, 7, 14, and 21 days after SCI. Results: At 7, 14, and 21 days after operation, the expression of the BDNF gene in the other 3 groups was higher than that of the NS group, and the difference was statistically significant ( P < .05). The apoptosis rate in the combined group was less than that of NS, EPO, and BDNF/BMSC groups, and the differences were statistically significant ( P < .05). Conclusion: Brain-derived neurotrophic factor gene-modified BMSC transplantation combined with EPO can promote the repair of nerve function after SCI in rats.


2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Donghe Han ◽  
Shurui Chen ◽  
Shiqiang Fang ◽  
Shiqiong Liu ◽  
Meihua Jin ◽  
...  

Muscle-derived stem cells (MDSCs) possess multipotent differentiation and self-renewal capacities; however, the effects and mechanism in neuron injury remain unclear. The aim of this study was to investigate the effects of MDSCs on neuron secondary injury, oxidative stress-induced apoptosis. An in vivo study showed the Basso, Beattie, and Bresnahan (BBB) score and number of neurons significantly increased after MDSCs’ transplantation in spinal cord injury (SCI) rats. An in vitro study demonstrated that MDSCs attenuated neuron apoptosis, and the expression of antioxidants was upregulated as well as the ratio of Bcl-2 and Bax in the MNT (MDSCs cocultured with injured neurons) group compared with the NT (injured neurons) group. Both LC3II/LC3I andβ-catenin were enhanced in the MNT group, while XAV939 (aβ-catenin inhibitor) decreased the expression of nuclear erythroid-related factor 2 (Nrf2) and LC3II/LC3I. Moreover, MDSCs became NSE- (neuron-specific enolase-) positive neuron-like cells with brain-derived neurotrophic factor (BDNF) treatment. The correlation analysis indicated that there was a significant relation between the level of BDNF and neuron injury. These findings suggest that MDSCs may protect the spinal cord from injury by inhibiting apoptosis and replacing injured neurons, and the increased BDNF andβ-catenin could contribute to MDSCs’ effects.


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