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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
Summary
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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