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

Published online by Cambridge University Press:  02 July 2020

H. Song ,
S. W. Downing  and
C. Wei
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
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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
Information
Microscopy and Microanalysis , Volume 6 , Issue S2: Proceedings: Microscopy & Microanalysis 2000, Microscopy Society of America 58th Annual Meeting, Microbeam Analysis Society 34th Annual Meeting, Microscopical Society of Canada/Societe de Microscopie de Canada 27th Annual Meeting, Philadelphia, Pennsylvania August 13-17, 2000 , August 2000 , pp. 630 - 631
Copyright
Copyright © Microscopy Society of America

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References

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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