P1061 Increased activity of the regulatory site of the calcineurin/NFAT pathway in human heart failure

2003 ◽  
Vol 24 (5) ◽  
pp. 187
Author(s):  
B BOLCK
Keyword(s):  
Heart Failure ◽  
Human Heart ◽  
Regulatory Site ◽  
Human Heart Failure ◽  
Increased Activity

Increased Cardiac Adrenergic Drive Precedes Generalized Sympathetic Activation in Human Heart Failure

Circulation ◽  
1997 ◽  
Vol 95 (1) ◽  
pp. 169-175 ◽  
Author(s):  
Bengt Rundqvist ◽  
Mikael Elam ◽  
Yrsa Bergmann-Sverrisdottir ◽  
Graeme Eisenhofer ◽  
Peter Friberg
Keyword(s):  
Heart Failure ◽  
Human Heart ◽  
Sympathetic Activation ◽  
Human Heart Failure

scholarly journals The Ku Protein Complex Interacts with YY1, Is Up-Regulated in Human Heart Failure, and Represses α Myosin Heavy-Chain Gene Expression

2004 ◽  
Vol 24 (19) ◽  
pp. 8705-8715 ◽  
Author(s):  
Carmen C. Sucharov ◽  
Steve M. Helmke ◽  
Stephen J. Langer ◽  
M. Benjamin Perryman ◽  
Michael Bristow ◽  
...  
Keyword(s):  
Heart Failure ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Human Heart ◽  
Ventricular Myocytes ◽  
Major Effect ◽  
Neonatal Rat ◽  
Chain Gene ◽  
Human Heart Failure ◽  
Peptide Mass

ABSTRACT Human heart failure is accompanied by repression of genes such as α myosin heavy chain (αMyHC) and SERCA2A and the induction of fetal genes such as βMyHC and atrial natriuretic factor. It seems likely that changes in MyHC isoforms contribute to the poor contractility seen in heart failure, because small changes in isoform composition can have a major effect on the contractility of cardiac myocytes and the heart. Our laboratory has recently shown that YY1 protein levels are increased in human heart failure and that YY1 represses the activity of the human αMyHC promoter. We have now identified a region of the αMyHC promoter that binds a factor whose expression is increased sixfold in failing human hearts. Through peptide mass spectrometry, we identified this binding activity to be a heterodimer of Ku70 and Ku80. Expression of Ku represses the human αMyHC promoter in neonatal rat ventricular myocytes. Moreover, overexpression of Ku70/80 decreases αMyHC mRNA expression and increases skeletal α-actin. Interestingly, YY1 interacts with Ku70 and Ku80 in HeLa cells. Together, YY1, Ku70, and Ku80 repress the αMyHC promoter to an extent that is greater than that with YY1 or Ku70/80 alone. Our results suggest that Ku is an important factor in the repression of the human αMyHC promoter during heart failure.

scholarly journals Quantitative mass spectral evidence for the absence of circulating brain natriuretic peptide (BNP-32) in severe human heart failure

2005 ◽  
Vol 102 (48) ◽  
pp. 17442-17447 ◽  
Author(s):  
A. M. Hawkridge ◽  
D. M. Heublein ◽  
H. R. Bergen ◽  
A. Cataliotti ◽  
J. C. Burnett ◽  
...  
Keyword(s):  
Heart Failure ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Human Heart ◽  
Human Heart Failure ◽  
Mass Spectral ◽  
Spectral Evidence
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