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Updated: Jul 13, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Calmodulin inhibitor-induced apoptosis was prevented by glycogen synthase kinase-3 inhibitors in PC12 cells

Tsuneo Takadera1, Takao Ohyashiki

  • 1Department of Clinical Chemistry, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan. t-takadera@hokuriku-u.ac.jp

Cellular and Molecular Neurobiology
|July 25, 2007
PubMed

Insights

Calmodulin inhibitors trigger programmed cell death (apoptosis) in PC12 cells, involving caspase activation and glycogen synthase kinase-3. Nerve growth factor blocks this cell death pathway.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Calmodulin (CaM) is a crucial calcium-binding protein that mediates intracellular calcium signals.
  • Understanding CaM's role in neuronal survival and death is vital for neurodegenerative disease research.

Purpose of the Study:

  • To investigate if calmodulin inhibitors induce apoptosis in PC12 cells.
  • To determine the involvement of glycogen synthase kinase-3 (GSK-3) in this process.

Main Methods:

  • PC12 cells were treated with W13 (a calmodulin inhibitor).
  • Apoptotic cell death was assessed via morphological changes and caspase-3 activation.
  • The effects of GSK-3 inhibitors, nerve growth factor (NGF), and cycloheximide were evaluated.

Main Results:

  • Calmodulin inhibition by W13 induced significant apoptotic cell death, characterized by cell shrinkage and nuclear fragmentation.
  • GSK-3 inhibitors attenuated W13-induced apoptosis.
  • NGF and cycloheximide completely prevented cell death, and NGF inhibited caspase-3 activation.

Conclusions:

  • Calmodulin inhibitors promote caspase-dependent apoptosis in PC12 cells.
  • Glycogen synthase kinase-3 activation plays a role in calmodulin inhibitor-induced neuronal cell death.

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