Abstract
When rat sciatic nerves are crushed, Schwann cells or other supporting cells distal to the injury site begin to synthesize and secrete an acidic 37-kilodalton (kDa) protein. This crush-induced protein accumulates within the nerve sheath and accounts for 2-5% of the total extracellular protein in the distal nerve stump. Synthesis of the 37-kDa protein increased for 2 weeks after nerve crush and declines slowly, beginning 4-6 weeks after the injury. The synthesis of the protein may be regulated by axon-Schwann cell contact. The specific induction of the 37-kDa protein and its accumulation in the extracellular space during nerve regeneration suggest that the protein promotes some aspect of axon growth. Because it is induced slowly after injury, the 37-kDa protein is unlikely to stimulate initial outgrowth of axons; however, it might promote later neuronal responses related to axon growth. The sciatic nerve supporting cells also respond to denervation by reducing the synthesis and release of two proteins of molecular mass 51 and 54 kDa. After crush injury to rat optic nerves, glial cells in the distal optic nerve stump also begin to synthesize and release an acidic 37-kDa protein, although axons of this central nervous system tract do not regenerate. If the 37-kDa protein from peripheral nerves proves to participate in the support of axon regrowth, then the results with rat optic nerve suggest that central nervous system glia initiate at least one part of an appropriate response to nerve injury.