Leucine-rich glioma inactivated 3 induces neurite outgrowth through Akt and focal adhesion kinase

Neurochem Res. 2010 May;35(5):789-96. doi: 10.1007/s11064-010-0136-0. Epub 2010 Feb 17.

Abstract

Leucine-rich glioma inactivated 3 (LGI3) is a secreted protein that belongs to LGI/epitempin family. LGI3 is highly expressed in brain in a transcriptionally and developmentally regulated manner. Here we found that LGI3 induced neurite outgrowth in Neuro-2a cells and dorsal root ganglia explants. LGI3 treatment or overexpression increased neurite outgrowth and knockdown of LGI3 by siRNA had opposite effect. LGI3 treatment increased phosphorylation of Akt and a 125-kDa protein. Immunoprecipitation identified the 125-kDa protein as focal adhesion kinase (FAK). LGI3 overexpression increased phospho-Akt, phospho-FAK and FAK protein. Inhibition of Akt activation by PI3 kinase inhibitor attenuated LGI3-induced FAK phosphorylation and neurite outgrowth. Taken together, we propose that LGI3 is a neuritogenic factor whose signaling pathway involves Akt-mediated FAK activation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Chromones / pharmacology
  • Focal Adhesion Protein-Tyrosine Kinases / physiology*
  • Ganglia, Spinal / growth & development
  • Mice
  • Morpholines / pharmacology
  • Nerve Tissue Proteins / physiology*
  • Neurites / drug effects
  • Neurites / physiology*
  • Phosphoinositide-3 Kinase Inhibitors
  • Proto-Oncogene Proteins c-akt / physiology*

Substances

  • Chromones
  • LGI3 protein, mouse
  • Morpholines
  • Nerve Tissue Proteins
  • Phosphoinositide-3 Kinase Inhibitors
  • 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
  • Focal Adhesion Protein-Tyrosine Kinases
  • Proto-Oncogene Proteins c-akt