Philadelphia, PA, September 29, 1998 -- Five years ago, Wistar Institute immunologist, Ellen Heber-Katz, Ph.D., and her Wistar research team identified a "healer" mouse capable of regenerating ear tissue. In a paper appearing today in the Proceedings of the National Academy of Sciences, they reveal their latest data on the genetics of the "healer" mouse.
Though still at the basic research stage, the Wistar scientists' findings are expected to have major implications for wound and burn healing, organ replacement, spinal cord regeneration and controlled tissue growth.
Because mice are genetically similar to humans, they are an ideal model for the laboratory study of mammalian regeneration. Prior to Dr. Heber-Katz's discovery of the "healer" mouse, it was possible to study regeneration only in amphibians, which are biologically, genetically and immunologically different from humans.
To collect information about the genetics of wound healing and regeneration, Dr. Heber-Katz and her group cross-bred "healer" mice with non-healers. It appears that, in inbred mice, this type of healing is a heritable trait.
By screening the entire mouse genome, Dr. Heber-Katz's laboratory, working in collaboration with immunogeneticist, Elizabeth Blankenhorn, Ph.D., of the Allegheny University of the Health Sciences, has identified multiple regions on five different chromosomes that appear to be responsible for wound healing and regeneration in mammals.
Although the researchers have not yet identified the precise contents of each locus, or region, one potential gene is a receptor for retinoic acid, known to play a role in developmental processes and the growth of skin. Interestingly, retinoic acid is also involved in amphibian regeneration.
Similar to what has been seen in amphibian regeneration, "healer" mice appear to
develop a blastema at the site of a wound. A blastema is a structure made up of
rapidly dividing immature cells with the potential to
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Contact: Diana Cutshall
dcutshall@wista.wistar.upenn.edu
(215) 898-3716
The Wistar Institute
30-Sep-1998