Human Nogo-C overexpression induces HEK293 cell apoptosis via a mechanism that involves JNK-c-Jun pathway

Biochem Biophys Res Commun. 2006 Sep 29;348(3):923-8. doi: 10.1016/j.bbrc.2006.07.166. Epub 2006 Aug 4.

Abstract

The neurite outgrowth inhibitor protein Nogo-A has been identified as an inhibitor of axonal regeneration, and Nogo-B as a regulator of vasculature remodeling, but the additional roles of Nogo isoforms, especially Nogo-C, have obtained little attention. Nogo-C is weakly expressed in liver and kidney compared to the high expression in skeletal muscle. Here we detected the weak expression of Nogo-C in human embryonic kidney cell line HEK293, and found that Nogo-C expressed in HEK293 could induce cell apoptosis. Further experiments demonstrated the activation of JNK/SAPK and c-Jun, but not p38 in Nogo-C expressed cells. And JNK-specific inhibitor SP600125 could reduce cell apoptosis induced by Nogo-C. Furthermore, the activation of caspase-3 and PARP, the expression and phosphorylation of p53 were also detected. The data first revealed Nogo-C expressed in HEK293 confers apoptosis by inducing caspase-3 and p53 activation through the JNK-c-Jun-dependent pathway.

MeSH terms

  • Apoptosis / genetics*
  • Caspase 3
  • Caspases / metabolism
  • Cell Line
  • Cloning, Molecular
  • Enzyme Activation / genetics
  • Humans
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • JNK Mitogen-Activated Protein Kinases / physiology*
  • Myelin Proteins / biosynthesis*
  • Myelin Proteins / genetics*
  • Myelin Proteins / physiology
  • Nogo Proteins
  • Protein Isoforms / genetics
  • Proto-Oncogene Proteins c-jun / physiology*
  • Signal Transduction / genetics*
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Myelin Proteins
  • Nogo Proteins
  • Protein Isoforms
  • Proto-Oncogene Proteins c-jun
  • RTN4 protein, human
  • Tumor Suppressor Protein p53
  • JNK Mitogen-Activated Protein Kinases
  • CASP3 protein, human
  • Caspase 3
  • Caspases