Serum withdrawal causes apoptosis in SHSY 5Y cells

Brain Res. 2001 Jan 19;889(1-2):308-15. doi: 10.1016/s0006-8993(00)03173-5.


A proportion of differentiated SH-SY5Y cells undergo cell death in response to withdrawal of serum. This death manifests the hallmark features of apoptosis including changes in nuclear morphology, processing and activation of caspase 3 and cleavage of the caspase 3 substrates acetyl-Asp-Glu-Val-Asp-aminomethylcoumarin and poly(ADP-ribose) polymerase. These findings represent the first demonstration of serum withdrawal induced apoptosis in SH-SY5Y cells. The reduction in viability induced by serum deprivation and assessed using an inhibitor of mitochondrial respiration can be partially inhibited by FK506, but FK506 does not prevent caspase 3 processing or cleavage of caspase 3 substrates. FK506 is also able to promote the viability of a small proportion of embryonic mouse sensory neurons following nerve growth factor-withdrawal induced apoptosis. FK506 did not promote viability in either cell type in the absence of serum- or nerve growth factor-withdrawal. These observations are consistent with a survival-promoting effect of FK506 in cultured neurons.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • Blotting, Western
  • Cell Survival / drug effects
  • Coumarins
  • Culture Media, Serum-Free
  • Fluorescent Dyes
  • Humans
  • Immunosuppressive Agents / pharmacology
  • Mice
  • Neurons / physiology*
  • Neurons, Afferent / drug effects
  • Oligopeptides
  • Tacrolimus / pharmacology
  • Trigeminal Ganglion / cytology
  • Trigeminal Ganglion / drug effects


  • Coumarins
  • Culture Media, Serum-Free
  • Fluorescent Dyes
  • Immunosuppressive Agents
  • Oligopeptides
  • acetyl-aspartyl-glutamyl-valyl-aspartyl-amino-4-methylcoumarin
  • Tacrolimus