Stem Cell Transplants Help Repair Spinal Cord Injuries in Rats
Nov. 29, 1999 (Indianapolis) -- Between 250,000 and 500,000 Americans have spinal cord injuries, and because many of them are young, they will spend decades in a wheelchair unless new treatments can be developed. Research in rats that is being reported in the December issue of the journal Nature Medicine may lead to new therapies in humans.
The neurons that make up the spinal cord have extensions, called axons, that resemble telephone wires and carry messages between the brain and the rest of the body. Traumatic injury can kill neurons or interrupt the axon connections, causing a loss of function. Unlike the heart, parts of the adult spinal cord do not survive transplantation.
In this study, the researchers used embryonic stem cells which have the potential to become any cell type in the body depending on what chemical signals they get when they mature. The researchers hoped that by triggering embryonic stem cells to become nerve cell precursors and then transplanting these precursor cells into the injured area they could promote healing of the spinal cord.
"Establishing regenerative therapies that promote substantial improvements in locomotion when instituted after the injury process is complete has been a difficult obstacle," says John W. McDonald, MD, PhD. McDonald is an assistant professor of neurology at Washington University School of Medicine in St. Louis. "This is a key threshold that had not before been crossed."
The researchers treated rats nine days after an injury to the spinal cord by transplanting stem cells from mice into the injury site. In another control group, the rats underwent a fake operation and were given only the culture medium with no cells.
Two to five weeks following the procedure, the researchers found various markers that showed the transplanted cells were alive and functioning. They also used special techniques to identify any axons that had grown from the transplanted cells. At two weeks, transplanted cells had not only filled the cavity at the point of injury, but had migrated up to 1 cm in each direction. By the five week follow-up, the cells were not as dense but the injured regions still contained mouse axons. None of the cells had developed into tumors.