N-acetylglucosaminyltranferase VB expression enhances beta1 integrin- dependent PC12 neurite outgrowth on laminin and collagen

J Neurochem. 2006 May;97(4):947-56. doi: 10.1111/j.1471-4159.2006.03785.x. Epub 2006 Apr 5.


N-acetylglucosaminyltransferase VB (GnT-VB, -IX) is a newly discovered glycosyltransferase expressed exclusively in high levels in neuronal tissue during early development. Its homolog, GnT-V, is expressed in many tissues and modulates cell-cell and cell-matrix adhesion. The ability of GnT-VB to regulate cell-matrix interactions was initially investigated using the rat pheochromocytoma PC12 neurite outgrowth model. PC12 cells stably transfected with GnT-VB consistently showed an enhanced rate of nerve growth factor (NGF)-induced neurite outgrowth on collagen and laminin substrates. Levels of TrkA receptor phosphorylation and downstream ERK activation induced by NGF were not influenced by GnT-VB expression. No significant difference was observed in the rate of neurite outgrowth when cells were cultured on non-coated culture dishes, indicating that integrin-ECM interaction is required for the stimulatory effects. Neurite outgrowth induced by manganese-dependent activation of beta1 integrin on collagen and laminin substrates, however, showed a significant increase in neurite length for the PC12/GnT-VB cells, compared with control cells, suggesting that the enhancement is most likely mediated by alteration of beta1 integrin-ECM interaction by GnT-VB. These results demonstrate that GnT-VB expression can modulate the rate of neurite outgrowth by affecting beta1 integrin-ECM interaction.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Cell Differentiation / drug effects
  • Cell Differentiation / physiology*
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Movement / physiology*
  • Collagen / metabolism
  • Collagen / pharmacology
  • Enzyme Activation / drug effects
  • Enzyme Activation / physiology
  • Extracellular Matrix / metabolism*
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Glycosylation / drug effects
  • Humans
  • Integrin beta1 / metabolism*
  • Laminin / metabolism
  • Laminin / pharmacology
  • Manganese / metabolism
  • Manganese / pharmacology
  • N-Acetylglucosaminyltransferases / genetics
  • N-Acetylglucosaminyltransferases / metabolism*
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism*
  • Neurites / drug effects
  • Neurites / metabolism*
  • PC12 Cells
  • Rats
  • Receptor, trkA / metabolism
  • Transfection
  • Up-Regulation / drug effects
  • Up-Regulation / physiology


  • Integrin beta1
  • Laminin
  • Nerve Tissue Proteins
  • Manganese
  • Collagen
  • MGAT5B protein, human
  • N-Acetylglucosaminyltransferases
  • Receptor, trkA
  • Extracellular Signal-Regulated MAP Kinases