SOX2 promotes spinal injury repair
Cells in some tissues of the body can multiply to replace dead or damaged cells after an injury, resulting in a healing effect. But studies have shown that spinal cords usually don't generate new neurons after an injury, which is a key barrier to recovery. Because the spinal cord serves as a signal relay between the brain and the rest of the body, its inability to repair itself can permanently disrupt communication between the two regions, leading to paralysis, loss of sensation and sometimes life threatening. Such as inability to control breathing or heart rhythm.
The researchers used a mouse model of spinal cord injury to look for markers normally found in immature neurons in the injured spinal cords of animals. The authors not only found this marker in the spinal cord after injury, but also tracked the cells that produced it: non-neuronal cells called NG2 glial cells.
NG2 glial cells are the cellular progenitors of oligodendrocytes, which produce the insulating layer of fat surrounding neurons. They are known to form colloidal scars after injury. Studies have shown that when spinal cord injury occurs, these glial cells temporarily adopt the molecular and morphological markers of immature neurons.
To determine what causes the changes in NG2 glial cells, the researchers focused on SOX2, a damage-induced stem cell protein. They genetically manipulated the cells to inactivate the gene that makes the protein. When the spinal cords of the manipulated mice were severed, the researchers saw far fewer immature neurons in the days after the injury, suggesting that SOX2 plays a key role in helping NG2 glial cells make these cells. However, even if SOX2 levels are normal, these immature neurons will never mature to replace the damaged neurons.
So the researchers used another genetic manipulation technique to overproduce SOX2 in NG2 glial cells. Excitingly, the mice that performed this procedure produced tens of thousands of new, mature neurons in the weeks after spinal cord injury. Further research showed that these neurons integrated into the injured area, making new connections with existing neurons, which are needed to carry signals between the brain and the body.
More hopefully, this genetic engineering has led to improved function after spinal cord injury. Animals engineered to produce excessive amounts of SOX2 in NG2 glia cells performed significantly better in motor skills weeks after spinal cord injury than animals that produced normal amounts of SOX2.
Eventually, researchers may be able to find safe and effective ways to overproduce SOX2 in human spinal cord injury patients, helping them repair the damage with new neurons while reducing the formation of scar tissue.
Wuxi Donglin Sci & Tech Development Co.,Ltd. has developed SOX2 ELISA Kits, if you want to know more about these kits, you can visit our website:
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The researchers used a mouse model of spinal cord injury to look for markers normally found in immature neurons in the injured spinal cords of animals. The authors not only found this marker in the spinal cord after injury, but also tracked the cells that produced it: non-neuronal cells called NG2 glial cells.
NG2 glial cells are the cellular progenitors of oligodendrocytes, which produce the insulating layer of fat surrounding neurons. They are known to form colloidal scars after injury. Studies have shown that when spinal cord injury occurs, these glial cells temporarily adopt the molecular and morphological markers of immature neurons.
To determine what causes the changes in NG2 glial cells, the researchers focused on SOX2, a damage-induced stem cell protein. They genetically manipulated the cells to inactivate the gene that makes the protein. When the spinal cords of the manipulated mice were severed, the researchers saw far fewer immature neurons in the days after the injury, suggesting that SOX2 plays a key role in helping NG2 glial cells make these cells. However, even if SOX2 levels are normal, these immature neurons will never mature to replace the damaged neurons.
So the researchers used another genetic manipulation technique to overproduce SOX2 in NG2 glial cells. Excitingly, the mice that performed this procedure produced tens of thousands of new, mature neurons in the weeks after spinal cord injury. Further research showed that these neurons integrated into the injured area, making new connections with existing neurons, which are needed to carry signals between the brain and the body.
More hopefully, this genetic engineering has led to improved function after spinal cord injury. Animals engineered to produce excessive amounts of SOX2 in NG2 glia cells performed significantly better in motor skills weeks after spinal cord injury than animals that produced normal amounts of SOX2.
Eventually, researchers may be able to find safe and effective ways to overproduce SOX2 in human spinal cord injury patients, helping them repair the damage with new neurons while reducing the formation of scar tissue.
Wuxi Donglin Sci & Tech Development Co.,Ltd. has developed SOX2 ELISA Kits, if you want to know more about these kits, you can visit our website:
http://www.dldevelop.com/Research-reagent/dl-sox2-ra.html
http://www.dldevelop.com/uploadfile/data/DL-SOX2-Ra.pdf
