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Presence of P53 and Transforming Growth Factor Beta-1 in Human Cardiac Tissue With Congestive Heart Failure

Published online by Cambridge University Press:  02 July 2020

Hong Song
Affiliation:
Cardiorenal Molecular Laboratory, University of Maryland School of Medicine, Baltimore, MD21201
Ren Shuxun
Affiliation:
Cardiorenal Molecular Laboratory, University of Maryland School of Medicine, Baltimore, MD21201
Xia Fen
Affiliation:
Cardiorenal Molecular Laboratory, University of Maryland School of Medicine, Baltimore, MD21201
Zhang Ruiwen
Affiliation:
Cardiorenal Molecular Laboratory, University of Maryland School of Medicine, Baltimore, MD21201
Wei Chi-Ming
Affiliation:
Cardiorenal Molecular Laboratory, University of Maryland School of Medicine, Baltimore, MD21201
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Extract

p53 is a tumor suppressor gene which involves apoptosis and cell cycle arrest under certain stress stimulate. The expression of p53 is associated with ischemia-reperfussion induced myocardial apoptosis in rat and with the development of coronary artery restenosis after angioplasty in humans. However, the status of p53 in human cardiomyocytes and fibroblasts in congestive heart failure (CHF) remains controversial.

Transforming growth factor-beta (TGF-β) is a growth-regulating peptide that has been shown to enhance collagen production both in vivo and in vitro in cultured cells. Both p53 and TGF-β may inhibit the cell growth and induce cellular apoptosis. While the previous studies demonstrated that TGF-β1 is present in the animal myocardium, the presentation and localization of TGF-β1 in human myocardium remain unclear.

Therefore, the present study was designed to investigate the p53 and TGF-β1 in human ventricular myocardium in normal subjects and in patients with heart failure. Five normal subjects and five end-stage failing human ventricular myocardium tissue were obtained from cardiac transplantation.

Type
Cytochemistry, Histochemistry, Immunocytochemistry, and in Situ Hybridization
Copyright
Copyright © Microscopy Society of America 1997

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References

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