Hostname: page-component-586b7cd67f-tf8b9 Total loading time: 0 Render date: 2024-11-26T09:35:43.214Z Has data issue: false hasContentIssue false

Angiotensin II Increases Apoptosis and Caspase-1 Expression in Human Myocardium

Published online by Cambridge University Press:  02 July 2020

H. Song
Affiliation:
Cardiovascular Molecular Research, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, 21201
S. W. Downing
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
Get access

Extract

Angiotensin II (AII) is a potent vasoconstrictor and mitogenic factor. The biological actions of All through AII receptors which include AT-1 and AT-2 receptors. However, the effects of AII on cardiomyocyte apoptosis and caspase expression remain controversial. Therefore, the current study was designed to investigate the actions of AII on human cardiomyocyte apoptosis and caspase-1 expression.

Human cardiac tissue was obtained from open-heart surgery (n=6). The cardiac tissue was minced and incubated in the special tissue culture system for 24 hours in the absence or presence of AII (10-7 M). These studies were repeated with losartan (10-6 M, AT-1 receptor antagonist) and PD123319 (PD, 10-6 M, AT-2 receptor antagonist). To detect the DNA fragmentation, TUNEL staining and DNA gel analyses were performed. The caspase-1 expression was determined by immunohistochemical staining (IHCS). An average of 1000 nuclei was analyzed for both TUNEL and caspase-1 IHCS studies.

Type
Apoptosis
Copyright
Copyright © Microscopy Society of America

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

References:

1.Wang, J., et al. Science (1996) 273, 359361.CrossRefGoogle Scholar
2.Goodfield, N.E., et al. Circulation (1999) 99, 29832985.CrossRefGoogle Scholar
3.Riegger, G.A., et al. Circulation (1999) 100, 22242230.CrossRefGoogle Scholar
4.Warnecke, C., et al. J Mol Med (1999) 77, 718727.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