Up-regulation of SKIP relates to retinal ganglion cells apoptosis after optic nerve crush in vivo

J Mol Histol. 2014 Dec;45(6):715-21. doi: 10.1007/s10735-014-9589-9. Epub 2014 Jul 30.

Abstract

Cell cycle re-entry is one of the key processes in neuronal apoptosis. Previous studies have shown that Ski-interacting protein (SKIP) played an important role in cell cycle re-entry. However, its expression and function in optic nerve injury are still with limited acquaintance. To investigate whether SKIP is involved in retinal ganglion cells (RGCs) death, we performed an optic nerve crush (ONC) model in adult rats. Western blot analysis revealed that up-regulation of SKIP was present in retina at 5 days after ONC. Immunofluorescent labeling indicated that up-regulated SKIP was found mainly in RGCs. We also investigated co-localization of SKIP with active-caspase-3 and TUNEL (apoptotic markers) -positive cells in the retina after ONC. In addition, the expression of SKIP was increased in parallel with P53 and P21 in retina after ONC. All these results suggested that up-regulation of SKIP in the retina was associated with RGCs death after ONC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Caspase 3 / metabolism
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • Gene Expression
  • Male
  • Nerve Crush
  • Optic Nerve / metabolism
  • Optic Nerve / pathology*
  • Rats, Sprague-Dawley
  • Retinal Ganglion Cells / physiology*
  • Transcription Factors / metabolism*
  • Tumor Suppressor Protein p53 / metabolism
  • Up-Regulation

Substances

  • Cyclin-Dependent Kinase Inhibitor p21
  • SKIP protein, rat
  • Transcription Factors
  • Tumor Suppressor Protein p53
  • Casp3 protein, rat
  • Caspase 3