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Decrease Tyrosine Phosphorylation of Stat3 in Human Myocardium with End-Stage Congestive Heart Failure

Published online by Cambridge University Press:  02 July 2020

C. Wei  and
J. S. McLaughlin
C. Wei
Affiliation:
Cardiovascular Molecular Research, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, 21201
J. S. McLaughlin
Affiliation:
Cardiovascular Molecular Research, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, 21201
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Extract

Recent study demonstrated that decrease signal transducer and activator of transcription-3 (STAT3) phosphorylation and increase apoptosis might be a critical point in the transition between compensatory cardiac hypertrophy and heart failure. To date, the protein expression of STAT3 in normal and failing human heart remains unclear. Therefore, the current study was designed to investigate the protein expression of STAT3 in human myocardium with end-stage congestive heart failure (CHF) and compared with that in normal human cardiac tissue.

Human cardiac atrial tissue was obtained from normal subjects (n=5) and end-stage CHF patients (n=5) during cardiac transplantation. To detect the DNA fragmentation, in situ terminal deoxymucleotidyl transferase dUTP nick end labeling (TUNEL) was performed. An average of 1000 nuclei was analyzed for TUNEL study. STAT3 protein expression and phosphorylation of STAT3 were determined by immunohistochemical staining (IHCS) with total STAT3 and phospho-specific STAT3 antibodies.

Type
Pathology
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. 596 - 597
Copyright
Copyright © Microscopy Society of America

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References

References:

1.Kunisada, K., et al. Circulation (1998) 98, 346–352.CrossRefGoogle Scholar
2.Fujio, Y., et al. J Clin Invest (1997) 99, 2898–2905.CrossRefGoogle Scholar
3.Kunisada, K., et al. Circulation (1996) 94, 2626–2632.CrossRefGoogle Scholar
4.Bromberg, J.F., et al. Cell (1999) 98, 295–303.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