Document Detail

Myocardial expression of survivin, an apoptosis inhibitor, in aging and heart failure. An experimental study in the spontaneously hypertensive rat.
MedLine Citation:
PMID:  16257070     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Apoptosis plays a major role in the transition to heart failure (HF) in systemic hypertension although the underlying mechanisms are still unclear. The aim of this study was to determine the relationship between apoptosis, left ventricular remodeling, heart failure and the myocyte expression of survivin, an inhibitor of apoptosis. METHODS: Spontaneously hypertensive rats (SHR) were used as a model of hypertensive cardiopathy, and Wistar Kyoto Stars rats (WKY) were used as controls. Animals were allowed to survive up to 18 months of age. The animals underwent echocardiography (EDD, ESD and FS were measured). The median section of the heart was processed for in situ end-labeling of DNA fragmentation (TUNEL) and for survivin expression by immunohistochemistry. RESULTS: All SHR presented features of adverse cardiac remodeling. Apoptotic cells were increased in SHR compared with WKY, measured as apoptotic cells per high power field (1.08+/-0.43 vs. 0.27+/-0.15, P<0.001), and as apoptotic rate (0.16+/-0.06% vs. 0.04+/-0.02%, P<0.001). The incidence of apoptosis showed a positive correlation with unfavorable ventricular remodeling, assessed by echocardiogram. Survivin expression was found in all cases, but the survivin expression index was significantly lower in SHR vs. WKY (43+/-40% vs. 86+/-18%, respectively, P=0.014). Moreover the survivin expression index was inversely correlated with features of adverse remodeling (i.e., Heart Weight, R=-0.79, P<0.001) and with apoptosis (i.e., apoptotic rate, R=-0.52, P=0.050). CONCLUSION: Survivin myocardial expression in aging SHR is associated with reduced apoptosis and more favorable cardiac remodeling. Modulation of this pathway may prove beneficial in preventing pressure overload cardiac remodeling and heart failure.
Antonio Abbate; Susanna Scarpa; Daniele Santini; Jimena Palleiro; Fortunata Vasaturo; John Miller; Celina Morales; George W Vetrovec; Alfonso Baldi
Publication Detail:
Type:  Journal Article     Date:  2005-10-27
Journal Detail:
Title:  International journal of cardiology     Volume:  111     ISSN:  0167-5273     ISO Abbreviation:  Int. J. Cardiol.     Publication Date:  2006 Aug 
Date Detail:
Created Date:  2006-08-18     Completed Date:  2007-01-03     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8200291     Medline TA:  Int J Cardiol     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  371-6     Citation Subset:  IM    
Department of Medicine, Virginia Commonwealth University, Richmond, VA, USA.
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MeSH Terms
Apoptosis / drug effects*,  physiology
Apoptosis Regulatory Proteins / metabolism*
Heart Failure / metabolism,  physiopathology*
Microtubule-Associated Proteins / metabolism*
Myocytes, Cardiac / metabolism*
Neoplasm Proteins / metabolism*
Rats, Inbred SHR
Rats, Inbred WKY
Ventricular Remodeling / drug effects,  physiology
Reg. No./Substance:
0/Apoptosis Regulatory Proteins; 0/BIRC5 protein, human; 0/Microtubule-Associated Proteins; 0/Neoplasm Proteins

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