Researchers at Karolinska Institutet have shown how the transplantation of stem cells improves recovery from spinal injury. However, a painful condition can also develop, which can be prevented if the stem cells are supplemented with a certain gene that controls their maturing process. The results are important for planning of stem cell therapy trials on patients with spinal injury.

Spinal injury confines some 150 Swedes a year to wheelchairs. The damage cause the loss of movement and sensation below the level of injury. A research team at Karolinska Institutet has now shown using rat models that the introduction of stem cells following such injury is effective, although a double-edged sword: while on the one hand the injection of stem cells into the damaged area of the spine improves motor function (movement) inferior to the injury level, scientists found that the rats developed greater pain sensitivity just superior of it.

In a follow-up study, a special gene, neurogenin-2, was added to the stem cells while they were developing in culture. When stem cells containing this gene were transplanted into the damaged spinal cord, the adverse pain effects failed to appear while the enhancement of motor function improved. Sensory function (feeling) below the injury also clearly improved.

The aggravated sensitivity to pain was thought to be the result of the fact that many stem cells developed into astrocytes, a kind of glial cell that encourages the growth of pain axons in the spinal cord by secreting substances that stimulate neuronal development.

The researchers found that the presence of neurogenin-2, a "transcription factor" that regulates the activity of other genes during the stem cell maturing process, inhibited the development of astrocytes and encouraged the formation of oligodendrocytes, another type of glial cell that forms the fatty myelin sheaths around the axons. The small number of astrocytes that developed from the neurogeni
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Contact: Professor Lars Olson
lars.olson@neuro.ki.se
46-8-524-870-50
Swedish Research Council
13-Feb-2005

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