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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

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

Tsuneo Takadera1, Yu Nakajima, Yuki Kanai

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

Cellular and Molecular Neurobiology
|March 20, 2010
PubMed

Insights

Glycogen synthase kinase-3 (GSK-3) inhibitors prevent colchicine-induced cell death in PC12 cells. This suggests GSK-3 activation plays a role in colchicine-induced apoptosis, a finding relevant to cell death research.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Colchicine is known to induce cell death.
  • The precise mechanisms of colchicine-induced apoptosis are not fully understood.
  • Glycogen synthase kinase-3 (GSK-3) is a key signaling enzyme implicated in various cellular processes.

Purpose of the Study:

  • To investigate the role of glycogen synthase kinase-3 (GSK-3) in colchicine-induced cell death.
  • To determine if GSK-3 inhibition can protect PC12 cells from colchicine toxicity.

Main Methods:

  • PC12 cells were treated with colchicine to induce cell death.
  • GSK-3 inhibitors (alsterpaullone, SB216763, AR-A014418) were used to block GSK-3 activity.
  • Morphological changes associated with apoptosis were observed.
  • Caspase-3 activation was measured as an indicator of apoptosis.

Main Results:

  • Colchicine induced significant apoptotic cell death in PC12 cells, evidenced by cell shrinkage and nuclear fragmentation.
  • Pre-treatment with GSK-3 inhibitors (alsterpaullone, SB216763, AR-A014418) effectively prevented colchicine-induced cell death.
  • GSK-3 inhibition also blocked the activation of caspase-3, a key executioner caspase in apoptosis.

Conclusions:

  • Colchicine triggers caspase-dependent apoptotic cell death in PC12 cells.
  • GSK-3 activation is critically involved in the pathway leading to colchicine-induced cell death.
  • Inhibiting GSK-3 offers a protective effect against colchicine toxicity in this cellular model.

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