Spatiotemporal dynamic changes, proliferation, and differentiation characteristics of Sox9-positive cells after severe complete transection spinal cord injury

2021 ◽  
Vol 337 ◽  
pp. 113556
Author(s):  
Haipeng Zhang ◽  
Weiwei Xue ◽  
Xiaoyu Xue ◽  
Yongheng Fan ◽  
Yaming Yang ◽  
...  
Author(s):  
Ronak Reshamwala ◽  
Tanja Eindorf ◽  
Megha Shah ◽  
Graham Smyth ◽  
Todd Shelper ◽  
...  

Spine ◽  
2011 ◽  
Vol 36 (25) ◽  
pp. 2130-2138 ◽  
Author(s):  
Jae Hwan Kim ◽  
Yong Woo Lee ◽  
Yu Mi Park ◽  
Kyung Ah Park ◽  
Seung Hwa Park ◽  
...  

2021 ◽  
Vol 16 (2) ◽  
pp. 382
Author(s):  
Bin Wang ◽  
Tian-Yun Gao ◽  
Fei-Fei Huang ◽  
Yuan-Yuan Xie ◽  
Wen-Qing Wang ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Fang Li ◽  
Mou-Wang Zhou ◽  
Nan Liu ◽  
Yan-Yan Yang ◽  
Hua-Yi Xing ◽  
...  

MicroRNA-219 (miR-219) regulates the proliferation and differentiation of oligodendrocyte precursor cells (OPCs) during central nervous system (CNS) development. OPCs only differentiate into oligodendrocytes (OLs) in the healthy CNS, but can generate astrocytes (As) after injury. We hypothesized that miR-219 may modulate OPC proliferation and differentiation in a cervical C5 contusion spinal cord injury (SCI) model. After injury, we observed a decrease in the miR-219 level and quantity of OLs and an increase in the number of OPCs and As. Silencing of miR-219 by its antagomir in vivo produced similar results, but of greater magnitude. Overexpression of miR-219 by its agomir in vivo increased the number of OLs and suppressed generation of OPCs and As. Luxol fast blue staining confirmed that SCI caused demyelination and that the extent of demyelination was attenuated by miR-219 overexpression, but aggravated by miR-219 reduction. Monocarboxylate transporter 1 (MCT-1) may be implicated in the regulation of OPC proliferation and differentiation mediated by miR-219 following contusion SCI. Collectively, our data suggest that miR-219 may mediate SCI-induced OPC proliferation and differentiation, and MCT-1 may participate in this process as a target of miR-219.


Biomaterials ◽  
2020 ◽  
Vol 237 ◽  
pp. 119830 ◽  
Author(s):  
Dezun Ma ◽  
Yannan Zhao ◽  
Lei Huang ◽  
Zhifeng Xiao ◽  
Bing Chen ◽  
...  

2014 ◽  
Vol 92 (5) ◽  
pp. 607-618 ◽  
Author(s):  
Carla Christina Medalha ◽  
Ying Jin ◽  
Takaya Yamagami ◽  
Christopher Haas ◽  
Itzhak Fischer

2019 ◽  
Vol 14 (5) ◽  
pp. 886 ◽  
Author(s):  
Ming-Liang Yang ◽  
Jian-Jun Li ◽  
Xin Zhang ◽  
Chang-Bin Liu ◽  
De-Gang Yang ◽  
...  

2022 ◽  
Vol 12 (3) ◽  
pp. 588-596
Author(s):  
Ming Xu ◽  
Guo Yong Tan ◽  
Xian Ming Tao

The major feature of spinal cord injury (SCI) was the damage of nervous tissue in spinal cord. The damaged spinal cord was difficult to be repaired and regenerated. MicroRNA-124 could play a role in the repairing and recovering the injured tissue. The BMSCs could participate in repairing the damage. However, the regulatory effect of MicroRNA-124 on BMSCs and the inflammatory response of SCI was still not illustrated. These spinal cord nerve cells were assigned into group of mechanical damage, BMSCs and BMSCs with miR-124 overexpression followed by analysis of proliferation of nerve cells by MTT assay, apoptotic activity, expression of miR-124, GFAP and BDNF by Real time PCR, levels of TNF-α and IL-6 by ELISA as well as MDH and SOD activity. miR-124 mimics transfection significantly promoted BMSCs proliferation and increased ALK activity and the expression of GFAP and BDNF. In conclusion, the proliferation and differentiation of BMSCs could be regulated by miR-124. The inflammation and oxidative stress could be restrained so as to prompt the proliferation and repair of SCI cells and restrain apoptosis, indicating that it might be beneficial to recover the SCI.


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