Format

Send to

Choose Destination
Invest Ophthalmol Vis Sci. 1997 Jun;38(7):1401-10.

The role of Schwann cells during retinal ganglion cell regeneration induced by peripheral nerve transplantation.

Author information

1
Department of Ophthalmology, Chiba University School of Medicine, Japan.

Abstract

PURPOSE:

To investigate the key role of Schwann cells in retinal ganglion cell regeneration elicited by peripheral nerve autotransplantation.

METHODS:

Three kinds of autografts, Schwann-cell graft (intact sciatic nerve, consisting of living Schwann cells and their basal laminae). Schwann-cell-eliminated graft (consisting mainly of Schwann cell basal laminae) and partial Schwann-cell graft (consisting of basal laminae and diffusible factors secreted by Schwann cells) were prepared and autotransplanted to the adult rat optic nerve. The membrane specialization between regenerating axons and Schwann cells was observed by electron microscopy. The expression of cell adhesion molecules was demonstrated by Western blot analysis and immunohistochemistry.

RESULTS:

Retinal ganglion cell axons were observed to regenerate into the Schwann-cell graft in contact with Schwann cells but not into the Schwann-cell-eliminated graft. The regeneration was not observed in the empty basal laminae of the partial Schwann-cell graft. Most of regenerating axons contacted astrocytes in the optic nerve segment, and Schwann cells in the graft. At the interface of regenerating axon and Schwann cell, in addition to immunoreactivity of N-CAM and LI, short focal tight junctions were observed.

CONCLUSIONS:

These results suggested that viable Schwann cells are good substrate for retinal ganglion cell regeneration, the intimate contact with viable Schwann cell surface plays an important role in retinal ganglion cell regeneration, tight junctions, and cell adhesion molecules (LI, N-CAM) are observed between the regenerating axon and Schwann cell.

PMID:
9191603
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Silverchair Information Systems
Loading ...
Support Center