Get access

Is the soluble KDI domain of γ1 laminin a regeneration factor for the mammalian central nervous system?

Authors

  • Ron Liebkind,

    1. The Brain Laboratory, Institute of Biomedicine (Anatomy), Biomedicum Helsinki, University of Helsinki, Helsinki, Finland
    Search for more papers by this author
  • Timo Laatikainen,

    1. Department of Obstetrics and Gynecology, Helsinki University Central Hospital, Maternity Hospital, Helsinki, Finland
    Search for more papers by this author
  • Päivi Liesi

    Corresponding author
    1. The Brain Laboratory, Institute of Biomedicine (Anatomy), Biomedicum Helsinki, University of Helsinki, Helsinki, Finland
    • The Brain Laboratory, Institute of Biomedicine (Anatomy), Biomedicum Helsinki, P.O. Box 63 (Haartmaninkatu 8), 00014 Helsinki, Finland
    Search for more papers by this author

Abstract

Regeneration of adult mammalian CNS is poor as a result of environmental factors that prevent axon growth. The major factors hampering regeneration of central axons include proteins released from the damaged myelin sheets of the injured neuronal pathways and formation of the glial scar. By using an experimental model of human CNS injury, we show that survival and neurite outgrowth of human central neurons are significantly enhanced by the soluble KDI domain of γ1 laminin. Our results indicate that the KDI domain appears to neutralize both glia-derived inhibitory signals and inhibitory molecules released from the myelin of the adult human spinal cord. We propose that the KDI domain may enhance regeneration of injuries in the adult mammalian CNS. © 2003 Wiley-Liss, Inc.

Ancillary