Document Detail

Severity of left ventricular dysfunction in heart failure patients affects the degree of serum-induced cardiomyocyte apoptosis. Importance of inflammatory response and metabolism.
MedLine Citation:
PMID:  22882964     Owner:  NLM     Status:  Publisher    
BACKGROUND/OBJECTIVES: In heart failure pro-inflammatory cytokines contribute to cardiomyocytes loss by apoptosis and play a role in the remodelling of the extracellular matrix (ECM). Myocardial injury recruits endothelial progenitor cells (EPCs) to the site of damage and stimulates their differentiation, contributing to myocardial tissue repair. We investigated if the severity of left ventricular dysfunction in heart failure patients (HF) may influence the ability of serum to induce cardiomyocytes death and whether this effect is affected by inflammation and intracellular oxidative stress pathways. METHODS: Adult murine cardiomyocytes HL-5 were incubated with 2% human serum from patients with heart failure (NYHA classes I to IV). Apoptosis was analysed by two different methods. TNF-α, IL-1β, IL-6, matrix metalloproteinase 1 (MMP-1) and tissue inhibitor of metalloproteinases 1 (TIMP-1) were measured in sera from patients. RESULTS: Cytokine levels were higher in sera from moderate-severe CHF compared to that of patients with mild CHF. Levels of CD117(+) (c-Kit(+)) cells and EPCs were significantly lower in blood from moderate-severe HF patients. Serum from HF patients induced a significantly higher ROS production involving p38 MAPK signalling and apoptosis in cardiomyocytes. NAC treatment prevented serum-induced oxidative effects. The increase of AMPK phosphorylation showed an involvement of FFA β-oxidation during apoptotic stress. CONCLUSIONS: All these alterations could be used as predictive factors of worsening in heart failure and culture of cardiomyocytes could be employed to test pharmacological effects.
Claudia Consoli; Lucia Gatta; Ferdinando Iellamo; Francesca Molinari; Giuseppe M C Rosano; Lionel N J L Marlier
Related Documents :
22080634 - A cardiac arrest: when recommended mild therapeutic hypothermia reveals the mechanism.
22293694 - Cardioprotective effect of fluvoxamine, sigma-1 receptor high affinity agonist.
2873274 - A method for evaluating antianginal drugs in experimental animals: assessment of myocar...
22347864 - Intracoronary levosimendan during ischemia prevents myocardial apoptosis.
17287644 - Effect of the arterial input function on the measured perfusion values and infarct volu...
22257804 - Percutaneous revascularization of total or subtotal left main occlusion in the setting ...
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-8-7
Journal Detail:
Title:  International journal of cardiology     Volume:  -     ISSN:  1874-1754     ISO Abbreviation:  Int. J. Cardiol.     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-8-13     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8200291     Medline TA:  Int J Cardiol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
Centre for Clinical & Basic Research, Cardiovascular Research Unit, Department. of Medical Sciences, IRCCS San Raffaele Pisana, Rome; Institute of Translational Pharmacology (IFT), National Research Council (CNR) Rome.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Acute aortic dissection: Epidemiology and outcomes.
Next Document:  Right to left shunting through communications between the left superior intercostal vein tributaries...