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Neuron regeneration plays a key role in maintaining brain homeostasis and responding to neurogenic injury.
However, the spinal cord of adult mammals lacks the ability to regenerate neurons.
Spinal cord injury can cause a variety of cell proliferations (including astrocytes, NG2 glial cells, microglia, fibroblasts, etc.
), but there is no definite in vivo experiment to prove that any of these cells can be found in the spinal cord.
It naturally transforms into mature neurons after injury.
On March 5, 2021, Zhang Chunli's group from the University of Texas Southwestern Medical Center and Xu Xiaoming's group from Indiana University School of Medicine jointly published the title in Cell Stem Cell Journal In vivo reprogramming of NG2 glia enables adult neurogenesis and functional recovery following spinal cord injury article.
This study revealed that NG2 glial cells have the potential to regenerate neurons after adult spinal cord injury.
They found that the high expression of endogenous SOX2 caused by spinal cord injury can cause NG2 glial cells to transform into DCX (a marker of neuron regeneration) positive cells, but they cannot further develop into mature neurons.
Interestingly, overexpression of exogenous SOX2 can successfully convert NG2 glial cells into functional neurons and promote functional repair in mice with spinal cord injury.
The researchers first observed the expression of DCX-positive cells after adult spinal cord injury.
They found that a large number of DCX-positive cells can be found around the spinal cord injury after 1 week of injury, and the number of such cells decreased sharply after 2 weeks of injury.
In order to determine the source of DCX-positive cells after spinal cord injury, a series of transgenic mice were used to track different cell types; it was found that the DCX-positive cells induced by spinal cord injury did not originate from ependymal cells or astrocytes, but It is derived from NG2 glial cells.
Therefore, it is determined that NG2 glial cells have the potential for nerve regeneration after adult spinal cord injury.
Next, the authors further studied the cellular and molecular mechanisms of NG2 glial cells in the transformation process.
The research group focused on the role of SOX2 in the transformation of NG2 glial cells into DCX-positive cells.
They found that SOX2 is mainly expressed in astrocytes and NG2 glial cells, while 94% of DCX-positive cells also express SOX2.
After conditionally knocking out SOX2 in astrocytes or NG2 glial cells, the researchers found that SOX2 is a sufficient and necessary condition for NG2 cells to transform into DCX-positive cells.
However, these DCX-positive cells cannot be successfully transformed into mature neurons.
Based on the SOX2 expression induced by spinal cord injury that can transform NG2 glial cells into DCX-positive cells, the researchers hypothesized that if SOX2 in NG2 glial cells is overexpressed with a viral system, whether NG2 cells can be transformed into mature functional nerves yuan.
The experimental results show that SOX2 overexpression can induce NG2 glial cells to reprogram and proliferate, and pass through the ASCL1 neural precursor stage, and transform into different subtypes (excitatory and inhibitory) mature nerves under the promotion of neurotrophic factors.
yuan.
The recombinant rabies virus system confirmed that these newly generated neurons can form extensive synaptic connections with neural pathways in the body.
Subsequently, the researchers used a spinal cord injury model to test whether in vivo reprogramming can improve the function after spinal cord injury.
Behavioral results show that reprogramming NG2 glial cells can significantly promote the forelimb motor function of mice after spinal cord injury.
Histological examination revealed that the newly generated neurons were mainly distributed around the lesion.
The three-dimensional reconstruction results of spinal cord glial scars showed that the volume and surface area of spinal cord scars were significantly reduced.
The author believes that the behavioral improvement after spinal cord injury may be related to the newly generated neurons and the improvement of the internal environment around the injury.
In the central nervous system, NG2 glial cells are the main source of oligodendrocytes.
Therefore, the authors also investigated whether the transformation of NG2 glial cells into neurons affects their differentiation into oligodendrocytes.
They found that reprogrammed NG2 glial cells have dual differentiation capabilities.
They can not only transform into mature neurons, but also into new oligodendrocytes.
In summary, this study revealed the plasticity of NG2 glial cells induced by adult spinal cord injury and the molecular mechanism of SOX2 overexpression.
By promoting the reprogramming of NG2 glial cells into neurons, the internal environment of spinal cord injury can be improved, which ultimately promotes the reconstruction and functional recovery of neural networks.
This research provides an important basis for the regeneration of adult spinal cord neurons and neural circuit reconstruction.
Original link: https://doi.
org/10.
1016/j.
stem.
2021.
02.
009 Plate maker: Notice for reprinting on the 11th The copyright of this article belongs to the author of the article.
Reprinting is prohibited without permission.
The author owns all legal rights, and offenders must be investigated.
.
However, the spinal cord of adult mammals lacks the ability to regenerate neurons.
Spinal cord injury can cause a variety of cell proliferations (including astrocytes, NG2 glial cells, microglia, fibroblasts, etc.
), but there is no definite in vivo experiment to prove that any of these cells can be found in the spinal cord.
It naturally transforms into mature neurons after injury.
On March 5, 2021, Zhang Chunli's group from the University of Texas Southwestern Medical Center and Xu Xiaoming's group from Indiana University School of Medicine jointly published the title in Cell Stem Cell Journal In vivo reprogramming of NG2 glia enables adult neurogenesis and functional recovery following spinal cord injury article.
This study revealed that NG2 glial cells have the potential to regenerate neurons after adult spinal cord injury.
They found that the high expression of endogenous SOX2 caused by spinal cord injury can cause NG2 glial cells to transform into DCX (a marker of neuron regeneration) positive cells, but they cannot further develop into mature neurons.
Interestingly, overexpression of exogenous SOX2 can successfully convert NG2 glial cells into functional neurons and promote functional repair in mice with spinal cord injury.
The researchers first observed the expression of DCX-positive cells after adult spinal cord injury.
They found that a large number of DCX-positive cells can be found around the spinal cord injury after 1 week of injury, and the number of such cells decreased sharply after 2 weeks of injury.
In order to determine the source of DCX-positive cells after spinal cord injury, a series of transgenic mice were used to track different cell types; it was found that the DCX-positive cells induced by spinal cord injury did not originate from ependymal cells or astrocytes, but It is derived from NG2 glial cells.
Therefore, it is determined that NG2 glial cells have the potential for nerve regeneration after adult spinal cord injury.
Next, the authors further studied the cellular and molecular mechanisms of NG2 glial cells in the transformation process.
The research group focused on the role of SOX2 in the transformation of NG2 glial cells into DCX-positive cells.
They found that SOX2 is mainly expressed in astrocytes and NG2 glial cells, while 94% of DCX-positive cells also express SOX2.
After conditionally knocking out SOX2 in astrocytes or NG2 glial cells, the researchers found that SOX2 is a sufficient and necessary condition for NG2 cells to transform into DCX-positive cells.
However, these DCX-positive cells cannot be successfully transformed into mature neurons.
Based on the SOX2 expression induced by spinal cord injury that can transform NG2 glial cells into DCX-positive cells, the researchers hypothesized that if SOX2 in NG2 glial cells is overexpressed with a viral system, whether NG2 cells can be transformed into mature functional nerves yuan.
The experimental results show that SOX2 overexpression can induce NG2 glial cells to reprogram and proliferate, and pass through the ASCL1 neural precursor stage, and transform into different subtypes (excitatory and inhibitory) mature nerves under the promotion of neurotrophic factors.
yuan.
The recombinant rabies virus system confirmed that these newly generated neurons can form extensive synaptic connections with neural pathways in the body.
Subsequently, the researchers used a spinal cord injury model to test whether in vivo reprogramming can improve the function after spinal cord injury.
Behavioral results show that reprogramming NG2 glial cells can significantly promote the forelimb motor function of mice after spinal cord injury.
Histological examination revealed that the newly generated neurons were mainly distributed around the lesion.
The three-dimensional reconstruction results of spinal cord glial scars showed that the volume and surface area of spinal cord scars were significantly reduced.
The author believes that the behavioral improvement after spinal cord injury may be related to the newly generated neurons and the improvement of the internal environment around the injury.
In the central nervous system, NG2 glial cells are the main source of oligodendrocytes.
Therefore, the authors also investigated whether the transformation of NG2 glial cells into neurons affects their differentiation into oligodendrocytes.
They found that reprogrammed NG2 glial cells have dual differentiation capabilities.
They can not only transform into mature neurons, but also into new oligodendrocytes.
In summary, this study revealed the plasticity of NG2 glial cells induced by adult spinal cord injury and the molecular mechanism of SOX2 overexpression.
By promoting the reprogramming of NG2 glial cells into neurons, the internal environment of spinal cord injury can be improved, which ultimately promotes the reconstruction and functional recovery of neural networks.
This research provides an important basis for the regeneration of adult spinal cord neurons and neural circuit reconstruction.
Original link: https://doi.
org/10.
1016/j.
stem.
2021.
02.
009 Plate maker: Notice for reprinting on the 11th The copyright of this article belongs to the author of the article.
Reprinting is prohibited without permission.
The author owns all legal rights, and offenders must be investigated.
.
