Regulation of Bartlett Endogenous Stem Cells in the Adult Mammalian Brain: Promoting Neuronal Repair

2003 ◽  
pp. 625-634
Author(s):  
Rodney L. Rietze ◽  
Perry F. Bartlett
2018 ◽  
Author(s):  
Sascha Dehler ◽  
Pak-Kin Lou ◽  
Maxim Skabkin ◽  
Sabrina Laudenklos ◽  
Andreas Neumann ◽  
...  

AbstractExternal stimuli such as injury, learning, or stress influence the production of neurons by neural stem cells (NSCs) in the adult mammalian brain. These external stimuli directly impact stem cell activity by influencing areas directly connected or in close proximity to the neurogenic niches of the adult brain. However, very little is known on how distant injuries affect NSC activation state. In this study we demonstrate that a thoracic spinal transection injury activates the distally located hippocampal-NSCs. This activation leads to a transient increase production of neurons that functionally integrate to improve animal’s performance in hippocampal-related memory tasks. We further show that interferon-CD95 signaling is required to promote injury-mediated activation of remote NSCs. Thus, we identify an immune-CNS axis responsible for injury-mediated activation of remotely located NSCs.


2006 ◽  
Vol 16 (suppl_1) ◽  
pp. i103-i111 ◽  
Author(s):  
B. Seri ◽  
D.G. Herrera ◽  
A. Gritti ◽  
S. Ferron ◽  
L. Collado ◽  
...  

2014 ◽  
Vol 2 (6) ◽  
pp. 810-824 ◽  
Author(s):  
Nadia Sachewsky ◽  
Rachel Leeder ◽  
Wenjun Xu ◽  
Keeley L. Rose ◽  
Fenggang Yu ◽  
...  

2021 ◽  
Author(s):  
Jayshree Samanta ◽  
James L. Salzer

ABSTRACTIn the adult mammalian brain, Gli1 expressing neural stem cells reside in the subventricular zone and their progeny are recruited to sites of demyelination in the white matter where they regenerate oligodendrocytes, the myelin forming cells. Remarkably, genetic loss or pharmacologic inhibition of Gli1 enhances the efficacy of remyelination by these neural stem cells. To understand the molecular mechanisms involved, we performed a transcriptomic analysis of this Gli1-pool of neural stem cells. We compared murine NSCs with either intact or deficient Gli1 expression from adult mice on a control diet or on a cuprizone diet to induce widespread demyelination. These data will be a valuable resource for identifying therapeutic targets for enhancing remyelination in demyelinating diseases like multiple sclerosis.


2000 ◽  
Vol 16 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Francisco Javier Rubio ◽  
Carlos Bueno ◽  
Ana Villa ◽  
Beatriz Navarro ◽  
Alberto Martı́nez-Serrano

2021 ◽  
Author(s):  
Daniel Z Radecki ◽  
Albert R Wang ◽  
Abigail S Johnson ◽  
Christian A Overman ◽  
Madison M Thatcher ◽  
...  

Gli1 expressing neural stem cells, in the subventricular zone of the adult mammalian brain, respond to demyelination injury by differentiating into oligodendrocytes. We have identified Gpnmb as a novel regulator of oligodendrogenesis in Gli1 neural stem cells, whose expression is induced by TGFβ1 signaling via Gli1, in response to a demyelinating injury. Upregulation of Gpnmb further activates the TGFβ1 pathway by increasing the expression of the TGFβ1 binding receptor subunit, TGFβR2. Thus the TGFβ1→Gli1→Gpnmb→TGFβR2 signaling pathway forms a feed forward loop for sustained activation of TGFβ1 signaling in Gli1 neural stem cells, resulting in inhibition of their differentiation into mature oligodendrocytes following demyelination.


2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Jayshree Samanta ◽  
Hernandez Moura Silva ◽  
Juan J. Lafaille ◽  
James L. Salzer

AbstractIn the adult mammalian brain, Gli1 expressing neural stem cells reside in the subventricular zone and their progeny are recruited to sites of demyelination in the white matter where they generate new oligodendrocytes, the myelin forming cells. Remarkably, genetic loss or pharmacologic inhibition of Gli1 enhances the efficacy of remyelination by these neural stem cells. To understand the molecular mechanisms involved, we performed a transcriptomic analysis of this Gli1-pool of neural stem cells. We compared murine NSCs with either intact or deficient Gli1 expression from adult mice on a control diet or on a cuprizone diet which induces widespread demyelination. These data will be a valuable resource for identifying therapeutic targets for enhancing remyelination in demyelinating diseases like multiple sclerosis.


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