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Bejarano I, Espino J, González-Flores D, et al. Role of Calcium Signals on Hydrogen Peroxide-Induced Apoptosis in Human Myeloid HL-60 Cells. Int J Biomed Sci. 2009;5(3):246-56
Bejarano, I., Espino, J., González-Flores, D., Casado, J. G., Redondo, P. C., Rosado, J. A., Barriga, C., Pariente, J. A., & Rodríguez, A. B. (2009). Role of Calcium Signals on Hydrogen Peroxide-Induced Apoptosis in Human Myeloid HL-60 Cells. International journal of biomedical science : IJBS, 5(3), 246-56.
Bejarano, Ignacio, et al. "Role of Calcium Signals on Hydrogen Peroxide-Induced Apoptosis in Human Myeloid HL-60 Cells." International journal of biomedical science : IJBS vol. 5,3 (2009): 246-56.
Bejarano I, Espino J, González-Flores D, Casado JG, Redondo PC, Rosado JA, Barriga C, Pariente JA, Rodríguez AB. Role of Calcium Signals on Hydrogen Peroxide-Induced Apoptosis in Human Myeloid HL-60 Cells. Int J Biomed Sci. 2009 Sep;5(3):246-56. PMID: 23675144; PMCID: PMC3614781.
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Int J Biomed Sci. 2009 Sep;5(3):246-56.

Role of Calcium Signals on Hydrogen Peroxide-Induced Apoptosis in Human Myeloid HL-60 Cells.

International journal of biomedical science : IJBS

Ignacio Bejarano, Javier Espino, David González-Flores, Javier G Casado, Pedro C Redondo, Juan A Rosado, Carmen Barriga, José A Pariente, Ana B Rodríguez

Affiliations

  1. Department of Physiology, University of Extremadura, Badajoz, Spain.

PMID: 23675144 PMCID: PMC3614781

Abstract

The present study is aimed to determine the role of calcium signaling evoked by the oxygen radical, hydrogen peroxide (H2O2) and the specific inhibitor of calcium reuptake thapsigargin on apoptosis in the human leukemia cell line HL-60. Our results show that treatment of HL-60 cells with 100 µM H2O2 and 1 µM thapsigargin induced a transient increase in cytosolic free calcium concentration ([Ca(2+)]c) due to calcium release from internal stores. These stimulatory effects on calcium signals were followed by activation of the mitochondrial permeability transition pore (mPTP), as well as a time-dependent increase in caspase-9 and -3 activities. Our results also show that H2O2 and thapsigargin were able to increase the relative content of fragmented DNA and phosphatidylserine externalization, as detected by double-staining with propidium iodide (PI) and annexin-V-FITC, respectively. Treatment of cells with H2O2 or thapsigargin resulted in activation of the proapoptotic protein Bid. Furthermore, coimmunoprecipitation experiments showed active Bax was bound to Bid, which regulates Bid activity and promotes apoptosis. Our findings suggest that H2O2(-) and thapsigargin-induced apoptosis is dependent on rises in [Ca(2+)]c in human myeloid HL-60 cells.

Keywords: H2O2; HL-60 cells; apoptosis; calcium signal; caspases; mitochondria

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