Centre for Medical Biology of Polish Academy of Sciences, Laboratory Transcriptional Regulation, 106 Lodowa Street, 93-232 Łódź, Poland.
Analysis of aclarubicin-induced cell death in human fibroblasts
Article first published online: 2 JAN 2013
© The Author(s) Journal compilation © 2007 International Federation for Cell Biology
Cell Biology International
Volume 31, Issue 9, pages 1049–1056, September 2007
How to Cite
Kania, K., Matławska-Wąsowska, K., Osiecka, R. and Jóźwiak, Z. (2007), Analysis of aclarubicin-induced cell death in human fibroblasts. Cell Biology International, 31: 1049–1056. doi: 10.1016/j.cellbi.2007.03.024
- Issue published online: 2 JAN 2013
- Article first published online: 2 JAN 2013
- Received 28 November 2005; revised 22 February 2007; accepted 21 March 2007
- Down's syndrome;
In the present study we investigated the mode of cell death induced by aclarubicin (ACL) in trisomic (BB) and normal (S-2) human fibroblasts. Cells were incubated with ACL for 2 h and then cultured in drug-free medium for up to 96 h. Using fluorescence microscopy, agarose gel electrophoresis and comet assay we demonstrate that ACL induced time-dependent morphological and biochemical changes in both cell types. The population of apoptotic cells, analysed by acridine orange and ethidium bromide nuclear staining reached its maximum at 24–48 h. Prolonged post-treatment time progressively increased the level of necrotic cells. At 24–48 h time points we also observed a significant increase in caspase-3 activity, oligonucleosomal DNA fragmentation and DNA strand breaks. Cotreatment of cells with the specific caspase-3 inhibitor Ac-DEVD-CHO partly reduced the extent of apoptosis and necrosis and DNA degradation. In conclusion, trisomic and normal fibroblasts demonstrate similar response to aclarubicin treatment. Drug induced the apoptotic and necrotic pathway of cell death that was mediated by caspase-3.