scholarly journals Effects and Mechanism of Action of Neonatal Versus Adult Astrocytes on Neural Stem Cell Proliferation After Traumatic Brain Injury

Stem Cells ◽  
2019 ◽  
Vol 37 (10) ◽  
pp. 1344-1356 ◽  
Author(s):  
Yong Dai ◽  
Feifan Sun ◽  
Hui Zhu ◽  
Qianqian Liu ◽  
Xide Xu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Brain Injury ◽  
Neural Stem Cell ◽  
Mechanism Of Action ◽  
Stem Cell Proliferation ◽  
Neural Stem Cell Proliferation

scholarly journals Adenosine kinase inhibition promotes proliferation of neural stem cells after traumatic brain injury

2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Hoda M Gebril ◽  
Rizelle Mae Rose ◽  
Raey Gesese ◽  
Martine P Emond ◽  
Yuqing Huo ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Brain Injury ◽  
Neural Stem Cell ◽  
Adenosine Kinase ◽  
Health Concern ◽  
Stem Cell Proliferation ◽  
Neural Stem Cell Proliferation ◽  
The Brain

Abstract Traumatic brain injury (TBI) is a major public health concern and remains a leading cause of disability and socio-economic burden. To date, there is no proven therapy that promotes brain repair following an injury to the brain. In this study, we explored the role of an isoform of adenosine kinase expressed in the cell nucleus (ADK-L) as a potential regulator of neural stem cell proliferation in the brain. The rationale for this hypothesis is based on coordinated expression changes of ADK-L during foetal and postnatal murine and human brain development indicating a role in the regulation of cell proliferation and plasticity in the brain. We first tested whether the genetic disruption of ADK-L would increase neural stem cell proliferation after TBI. Three days after TBI, modelled by a controlled cortical impact, transgenic mice, which lack ADK-L (ADKΔneuron) in the dentate gyrus (DG) showed a significant increase in neural stem cell proliferation as evidenced by significant increases in doublecortin and Ki67-positive cells, whereas animals with transgenic overexpression of ADK-L in dorsal forebrain neurons (ADK-Ltg) showed an opposite effect of attenuated neural stem cell proliferation. Next, we translated those findings into a pharmacological approach to augment neural stem cell proliferation in the injured brain. Wild-type C57BL/6 mice were treated with the small molecule adenosine kinase inhibitor 5-iodotubercidin for 3 days after the induction of TBI. We demonstrate significantly enhanced neural stem cell proliferation in the DG of 5-iodotubercidin-treated mice compared to vehicle-treated injured animals. To rule out the possibility that blockade of ADK-L has any effects in non-injured animals, we quantified baseline neural stem cell proliferation in ADKΔneuron mice, which was not altered, whereas baseline neural stem cell proliferation in ADK-Ltg mice was enhanced. Together these findings demonstrate a novel function of ADK-L involved in the regulation of neural stem cell proliferation after TBI.

Exercise increases neural stem cell proliferation surrounding the area of damage following rat traumatic brain injury

2010 ◽  
Vol 118 (2) ◽  
pp. 193-202 ◽  
Author(s):  
Tatsuki Itoh ◽  
Motohiro Imano ◽  
Shozo Nishida ◽  
Masahiro Tsubaki ◽  
Shigeo Hashimoto ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Brain Injury ◽  
Neural Stem Cell ◽  
Stem Cell Proliferation ◽  
Neural Stem Cell Proliferation

Could the endogenous opioid, morphine, prevent neural stem cell proliferation?

2011 ◽  
Vol 76 (2) ◽  
pp. 225-229 ◽  
Author(s):  
Alireza Shoae-Hassani ◽  
Shiva Sharif ◽  
Seyed Abdolreza Mortazavi Tabatabaei ◽  
Javad Verdi
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Neural Stem Cell ◽  
Endogenous Opioid ◽  
Stem Cell Proliferation ◽  
Neural Stem Cell Proliferation
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