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Cyclosporine-Induced Apoptosis in Human Cardiomyocytes Through P53-Dependent Pathway

Published online by Cambridge University Press:  02 July 2020

M. Kinjo
Affiliation:
Cardiovascular Molecular Research, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, 21201
C. Wei
Affiliation:
Cardiovascular Molecular Research, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, 21201
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Extract

Cyclosporine A (CsA) is the most effective and widely used immunosuppressant drug in heart, lung and kidney transplantation. However, the effect of CsA is limited by the significant toxicity. The mechanism of CsA-induced toxicity is remaining controversial. Cellular apoptosis is being suggested as a possible mediator of CsA toxicity. To date, regarding the effects of CsA on apoptosis and apoptosis-related gene regulation in cardiomyocytes remain unclear. Therefore, the current study was designed to investigate the effect of CsA on apoptosis and apoptosis-related gene p53 expression in human cardiomyocytes. We hypothesized that CsA induces apoptosis in human cardiomyocytes through p53-dependent pathway.

Human cardiac atrial tissue was obtained from open-heart surgery (n=5). The cardiac tissue was minced and incubated in the special tissue culture system for 24 hours in the absence or presence of CsA (10-7 M). To detect the DNA fragmentation, in situ terminal deoxymucleotidyl transferase dUTP nick end labeling (TUNEL) was performed.

Type
Apoptosis
Copyright
Copyright © Microscopy Society of America

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References

References:

1.Soares, M. P., et al. Nat Med. (1998) 4, 10731077.CrossRefGoogle Scholar
2.Vriens, P. W., et al. J Thorac Cardiovasc Surg (1998) 116, 844853.CrossRefGoogle Scholar
3.Jurado, F., et al. Histol Histopathol (1999) 14, 10331043.Google Scholar
4.Morgan, D. C., et al. Circulation (1999) 100, 12361241.CrossRefGoogle Scholar
5. This research was supported in part by grants from the NIH (HL03174 & HL61299, C. Wei), AHAMD, NKF and University of Maryland School of Medicine.Google Scholar