An endogenous lectin and its glycoprotein ligands are triggering basal and axon-induced Schwann cell proliferation

Glycobiology. 1995 Jun;5(4):371-83. doi: 10.1093/glycob/5.4.371.

Abstract

The proliferation of Schwann cells (the myelinating cells of the peripheral nervous system) is stimulated by the contact with axonal membranes. It is suggested that the endogenous carbohydrate-binding protein (lectin) cerebellar soluble lectin (CSL) bound to ligands at the surface of axonal preparations is mitogenic for Schwann cells. Both autocrine and axon-stimulated Schwann cell proliferations seem to be dependent on the presence of CSL and its ligands at the Schwann cell surface, as suggested by the effects of N-glycosylation inhibitors and anti-CSL Fab fragments. These data suggest that CSL regulates Schwann cell proliferation by clustering of a few glycoprotein ligands at the cell surface, consequently modulating phosphorylations.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1-Deoxynojirimycin / pharmacology
  • Animals
  • Axons / physiology*
  • Cell Division / drug effects
  • Cell Division / physiology*
  • Cells, Cultured
  • Enzyme Inhibitors / pharmacology
  • Glycoproteins / analysis
  • Glycoproteins / metabolism
  • Glycoproteins / pharmacology*
  • Glycosylation
  • Lectins / analysis
  • Lectins / pharmacology*
  • Lectins / physiology
  • Mitogens / pharmacology*
  • Rats
  • Schwann Cells / chemistry
  • Schwann Cells / cytology*
  • Swainsonine / pharmacology
  • Tunicamycin / pharmacology

Substances

  • Enzyme Inhibitors
  • Glycoproteins
  • Lectins
  • Mitogens
  • cerebellar soluble lectin
  • Tunicamycin
  • 1-Deoxynojirimycin
  • Swainsonine