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Tacrolimus-Induced Apoptosis is Mediated by Endoplasmic Reticulum-derived Calcium-dependent Caspases-3,-12 in Jurkat

Y W Chung1, M W Chung2, S K Choi2

  • 1Department of Surgery, Chonnam National University Medical School, Gwangju, Korea.

Transplantation Proceedings
|May 8, 2018
PubMed

Insights

Tacrolimus induces apoptosis in Jurkat cells by increasing intracellular calcium and activating caspases-3 and -12. This endoplasmic reticulum stress pathway is crucial for Tac-induced cell death.

Area of Science:

  • Immunology
  • Cell Biology
  • Pharmacology

Background:

  • Apoptosis involves various pathways, including the endoplasmic reticulum (ER) pathway, which can be initiated by caspases.
  • Tacrolimus (Tac) is known to induce apoptosis, characterized by nuclear fragmentation and caspase-3 activation.

Purpose of the Study:

  • To investigate the role of ER-derived calcium and specific caspases (caspase-3 and caspase-12) in Tacrolimus-induced apoptosis in Jurkat human T lymphocytes.

Main Methods:

  • Jurkat cells were treated with varying concentrations of Tacrolimus.
  • Intracellular calcium levels were measured using calcium ionophore (A23187) and calcium adenosine triphosphatase inhibitor (thapsigargin).
  • The activity of caspases-3, -6, -8, -9, and -12 was assessed.

Main Results:

  • Tacrolimus decreased Jurkat cell viability in a dose-dependent manner.
  • Tacrolimus treatment led to a continuous increase in intracellular calcium concentration over 72 hours.
  • Tacrolimus induced the activation of caspase-12 and caspase-3, but not caspase-6, -8, or -9.

Conclusions:

  • Tacrolimus-induced apoptosis in Jurkat cells is mediated by ER-derived calcium.
  • The activation of caspase-3 and caspase-12 plays a key role in this Tacrolimus-induced apoptotic pathway.

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