"Through molecular signals, the injury spreads throughout the spinal cord," said Pamela Knapp, Ph.D., assistant professor, Department of Anatomy and Neurobiology, UK College of Medicine, and co-author of the paper. "The oligodendroglia, although undamaged by the original injury, can die in the weeks following the trauma. By developing therapeutic strategies that can prevent the death of the oligodendroglia by inhibiting the apoptotic molecular pathway, we hope to promote nerve function and improve recovery from spinal cord injury."

The caspase family of proteases, enzymes that destroy proteins by breaking them into individual amino acids, regulates apoptosis in humans and other mammals. This research clearly shows that in cells that are damaged by spinal cord injuries, the release of a protein called cytochrome c from the mitochondria causes the proteins Apaf-1 and procaspase-9 to bind together. This, in turn, activates caspase-3 which then cleaves several proteins (gelsolin, PAK2, fodrin, and DFF40/CAD), resulting in DNA fragmentation and destruction of the cellular structure. These molecular signals then spread to surrounding areas of the spinal cord.

This research project was one of the first supported by the Kentucky Spinal Cord and Head Injury Research Trust (KSCHIRT). Established by the 1994 General Assembly of the Commonwealth of Kentucky, KSCHIRT allocates funds to support spinal cord and head injury research at UK and the University of Louisville with the major goals of understanding how cells die following head or spinal cord injury and identifying effective therapeutic treatments.

"The UK Chandler Medical Center has several established clinical and basic scientists investigating spinal cord and head injury," Springer said. "With continued support from KSCHIRT and other funding organizations, the UK Chandler Medical Center cl
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Contact: Maureen McArthur
mhmcar2@pop.uky.edu
606-323-6363
University of Kentucky Medical Center
27-Jul-1999