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Cyclosporine inhibited calcium-mediated apoptosis of HL-60 cells

Q Q Huang1, M Fang, H Q Zhang

  • 1Department of Biology, Beijing Normal University, China.

Zhongguo Yao Li Xue Bao = Acta Pharmacologica Sinica
|May 1, 1997
PubMed

Insights

Cyclosporine (Cyc) inhibits apoptosis in HL-60 cells only when it is induced by increased intracellular calcium. This suggests distinct mechanisms for apoptosis triggered by calcium-increasing agents versus others like harringtonine or camptothecin.

Area of Science:

  • Cell Biology
  • Pharmacology

Background:

  • Apoptosis, or programmed cell death, is a critical cellular process.
  • Understanding the modulators of apoptosis is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the impact of cyclosporine (Cyc) on apoptosis in HL-60 cells.
  • To determine if Cyc affects apoptosis induced by various agents and explore the role of intracellular calcium.

Main Methods:

  • HL-60 cells were induced to undergo apoptosis using harringtonine (Har), camptothecin (Cam), calcimycin (Cal), or thapsigargin (Tha).
  • Apoptosis was assessed via DNA electrophoresis, cell morphology, and flow cytometry.
  • Intracellular calcium levels ([Ca2+]i) in apoptotic cells were measured using flow cytometry.

Main Results:

  • Calcimycin (Cal) and thapsigargin (Tha) induced apoptosis in HL-60 cells, accompanied by an increase in intracellular calcium.
  • Cyclosporine (Cyc) at a nontoxic concentration inhibited apoptosis induced by Cal and Tha.
  • Cyc did not affect apoptosis induced by Har or Cam, which did not alter intracellular calcium levels.

Conclusions:

  • Cyclosporine (Cyc) selectively inhibits apoptosis in HL-60 cells when the process is mediated by increased intracellular calcium.
  • The mechanisms of apoptosis induced by calcium-increasing agents (Cal, Tha) differ from those induced by Har or Cam.
Abstract

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